TY  - JOUR
AU  - Grigorov, Ilijana
AU  - Pejić, Snežana
AU  - Todorović, Ana
AU  - Drakulić, Dunja
AU  - Veljković, Filip
AU  - Miletić Vukajlović, Jadranka
AU  - Bobić, Katarina
AU  - Soldatović, Ivan
AU  - Đurašević, Siniša
AU  - Jasnić, Nebojša
AU  - Stanković, Sanja
AU  - Glumac, Sofija
AU  - Mihailović-Vučinić, Violeta
AU  - Milenković, Branislava
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11550
AB  - The careful monitoring of patients with mild/moderate COVID-19 is of particular importance because of the rapid progression of complications associated with COVID-19. For prognostic reasons and for the economic management of health care resources, additional biomarkers need to be identified, and their monitoring can conceivably be performed in the early stages of the disease. In this retrospective cross-sectional study, we found that serum concentrations of high-mobility group box 1 (HMGB1) and heme oxygenase-1 (HO-1), at the time of hospital admission, could be useful biomarkers for COVID-19 management. The study included 160 randomly selected recovered patients with mild to moderate COVID-19 on admission. Compared with healthy controls, serum HMGB1 and HO-1 levels increased by 487.6 pg/mL versus 43.1 pg/mL and 1497.7 pg/mL versus 756.1 pg/mL, respectively. Serum HO-1 correlated significantly with serum HMGB1, oxidative stress parameters (malondialdehyde (MDA), the phosphatidylcholine/lysophosphatidylcholine ratio (PC/LPC), the ratio of reduced and oxidative glutathione (GSH/GSSG)), and anti-inflammatory acute phase proteins (ferritin, haptoglobin). Increased heme catabolism/hemolysis were not detected. We hypothesize that the increase in HO-1 in the early phase of COVID-19 disease is likely to have a survival benefit by providing protection against oxidative stress and inflammation, whereas the level of HMGB1 increase reflects the activity of the innate immune system and represents levels within which the disease can be kept under control.
T2  - International Journal of Molecular Sciences
T1  - Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission
VL  - 24
IS  - 17
SP  - 13164
DO  - 10.3390/ijms241713164
ER  - 

@article{
author = "Grigorov, Ilijana and Pejić, Snežana and Todorović, Ana and Drakulić, Dunja and Veljković, Filip and Miletić Vukajlović, Jadranka and Bobić, Katarina and Soldatović, Ivan and Đurašević, Siniša and Jasnić, Nebojša and Stanković, Sanja and Glumac, Sofija and Mihailović-Vučinić, Violeta and Milenković, Branislava",
year = "2023",
abstract = "The careful monitoring of patients with mild/moderate COVID-19 is of particular importance because of the rapid progression of complications associated with COVID-19. For prognostic reasons and for the economic management of health care resources, additional biomarkers need to be identified, and their monitoring can conceivably be performed in the early stages of the disease. In this retrospective cross-sectional study, we found that serum concentrations of high-mobility group box 1 (HMGB1) and heme oxygenase-1 (HO-1), at the time of hospital admission, could be useful biomarkers for COVID-19 management. The study included 160 randomly selected recovered patients with mild to moderate COVID-19 on admission. Compared with healthy controls, serum HMGB1 and HO-1 levels increased by 487.6 pg/mL versus 43.1 pg/mL and 1497.7 pg/mL versus 756.1 pg/mL, respectively. Serum HO-1 correlated significantly with serum HMGB1, oxidative stress parameters (malondialdehyde (MDA), the phosphatidylcholine/lysophosphatidylcholine ratio (PC/LPC), the ratio of reduced and oxidative glutathione (GSH/GSSG)), and anti-inflammatory acute phase proteins (ferritin, haptoglobin). Increased heme catabolism/hemolysis were not detected. We hypothesize that the increase in HO-1 in the early phase of COVID-19 disease is likely to have a survival benefit by providing protection against oxidative stress and inflammation, whereas the level of HMGB1 increase reflects the activity of the innate immune system and represents levels within which the disease can be kept under control.",
journal = "International Journal of Molecular Sciences",
title = "Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission",
volume = "24",
number = "17",
pages = "13164",
doi = "10.3390/ijms241713164"
}

Grigorov, I., Pejić, S., Todorović, A., Drakulić, D., Veljković, F., Miletić Vukajlović, J., Bobić, K., Soldatović, I., Đurašević, S., Jasnić, N., Stanković, S., Glumac, S., Mihailović-Vučinić, V.,& Milenković, B.. (2023). Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission. in International Journal of Molecular Sciences, 24(17), 13164.
https://doi.org/10.3390/ijms241713164

Grigorov I, Pejić S, Todorović A, Drakulić D, Veljković F, Miletić Vukajlović J, Bobić K, Soldatović I, Đurašević S, Jasnić N, Stanković S, Glumac S, Mihailović-Vučinić V, Milenković B. Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission. in International Journal of Molecular Sciences. 2023;24(17):13164.
doi:10.3390/ijms241713164 .

Grigorov, Ilijana, Pejić, Snežana, Todorović, Ana, Drakulić, Dunja, Veljković, Filip, Miletić Vukajlović, Jadranka, Bobić, Katarina, Soldatović, Ivan, Đurašević, Siniša, Jasnić, Nebojša, Stanković, Sanja, Glumac, Sofija, Mihailović-Vučinić, Violeta, Milenković, Branislava, "Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission" in International Journal of Molecular Sciences, 24, no. 17 (2023):13164,
https://doi.org/10.3390/ijms241713164 . .

TY  - JOUR
AU  - Zeljković Jovanović, Milica
AU  - Stanojević, Jelena
AU  - Stevanović, Ivana
AU  - Stekić, Anđela
AU  - Bolland, Samuel J.
AU  - Jasnić, Nebojša
AU  - Ninković, Milica
AU  - Zarić Kontić, Marina
AU  - Ilić, Tihomir V.
AU  - Rodger, Jennifer
AU  - Nedeljković, Nadežda
AU  - Dragić, Milorad
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11099
AB  - Parkinson’s disease (PD) is the second most common neurodegenerative disorder characterized by the progressive degeneration of the dopaminergic system, leading to a variety of motor and nonmotor symptoms. The currently available symptomatic therapy loses efficacy over time, indicating the need for new therapeutic approaches. Repetitive transcranial magnetic stimulation (rTMS) has emerged as one of the potential candidates for PD therapy. Intermittent theta burst stimulation (iTBS), an excitatory protocol of rTMS, has been shown to be beneficial in several animal models of neurodegeneration, including PD. The aim of this study was to investigate the effects of prolonged iTBS on motor performance and behavior and the possible association with changes in the NMDAR subunit composition in the 6-hydroxydopamine (6-OHDA)-induced experimental model of PD. Two-month-old male Wistar rats were divided into four groups: controls, 6-OHDA rats, 6-OHDA + iTBS protocol (two times/day/three weeks) and the sham group. The therapeutic effect of iTBS was evaluated by examining motor coordination, balance, spontaneous forelimb use, exploratory behavior, anxiety-like, depressive/anhedonic-like behavior and short-term memory, histopathological changes and changes at the molecular level. We demonstrated the positive effects of iTBS at both motor and behavioral levels. In addition, the beneficial effects were reflected in reduced degeneration of dopaminergic neurons and a subsequent increase in the level of DA in the caudoputamen. Finally, iTBS altered protein expression and NMDAR subunit composition, suggesting a sustained effect. Applied early in the disease course, the iTBS protocol may be a promising candidate for early-stage PD therapy, affecting motor and nonmotor deficits. © 2023 by the authors.
T2  - Cells
T1  - Intermittent Theta Burst Stimulation Improves Motor and Behavioral Dysfunction through Modulation of NMDA Receptor Subunit Composition in Experimental Model of Parkinson’s Disease
VL  - 12
IS  - 11
DO  - 10.3390/cells12111525
ER  - 

@article{
author = "Zeljković Jovanović, Milica and Stanojević, Jelena and Stevanović, Ivana and Stekić, Anđela and Bolland, Samuel J. and Jasnić, Nebojša and Ninković, Milica and Zarić Kontić, Marina and Ilić, Tihomir V. and Rodger, Jennifer and Nedeljković, Nadežda and Dragić, Milorad",
year = "2023",
abstract = "Parkinson’s disease (PD) is the second most common neurodegenerative disorder characterized by the progressive degeneration of the dopaminergic system, leading to a variety of motor and nonmotor symptoms. The currently available symptomatic therapy loses efficacy over time, indicating the need for new therapeutic approaches. Repetitive transcranial magnetic stimulation (rTMS) has emerged as one of the potential candidates for PD therapy. Intermittent theta burst stimulation (iTBS), an excitatory protocol of rTMS, has been shown to be beneficial in several animal models of neurodegeneration, including PD. The aim of this study was to investigate the effects of prolonged iTBS on motor performance and behavior and the possible association with changes in the NMDAR subunit composition in the 6-hydroxydopamine (6-OHDA)-induced experimental model of PD. Two-month-old male Wistar rats were divided into four groups: controls, 6-OHDA rats, 6-OHDA + iTBS protocol (two times/day/three weeks) and the sham group. The therapeutic effect of iTBS was evaluated by examining motor coordination, balance, spontaneous forelimb use, exploratory behavior, anxiety-like, depressive/anhedonic-like behavior and short-term memory, histopathological changes and changes at the molecular level. We demonstrated the positive effects of iTBS at both motor and behavioral levels. In addition, the beneficial effects were reflected in reduced degeneration of dopaminergic neurons and a subsequent increase in the level of DA in the caudoputamen. Finally, iTBS altered protein expression and NMDAR subunit composition, suggesting a sustained effect. Applied early in the disease course, the iTBS protocol may be a promising candidate for early-stage PD therapy, affecting motor and nonmotor deficits. © 2023 by the authors.",
journal = "Cells",
title = "Intermittent Theta Burst Stimulation Improves Motor and Behavioral Dysfunction through Modulation of NMDA Receptor Subunit Composition in Experimental Model of Parkinson’s Disease",
volume = "12",
number = "11",
doi = "10.3390/cells12111525"
}

Zeljković Jovanović, M., Stanojević, J., Stevanović, I., Stekić, A., Bolland, S. J., Jasnić, N., Ninković, M., Zarić Kontić, M., Ilić, T. V., Rodger, J., Nedeljković, N.,& Dragić, M.. (2023). Intermittent Theta Burst Stimulation Improves Motor and Behavioral Dysfunction through Modulation of NMDA Receptor Subunit Composition in Experimental Model of Parkinson’s Disease. in Cells, 12(11).
https://doi.org/10.3390/cells12111525

Zeljković Jovanović M, Stanojević J, Stevanović I, Stekić A, Bolland SJ, Jasnić N, Ninković M, Zarić Kontić M, Ilić TV, Rodger J, Nedeljković N, Dragić M. Intermittent Theta Burst Stimulation Improves Motor and Behavioral Dysfunction through Modulation of NMDA Receptor Subunit Composition in Experimental Model of Parkinson’s Disease. in Cells. 2023;12(11).
doi:10.3390/cells12111525 .

Zeljković Jovanović, Milica, Stanojević, Jelena, Stevanović, Ivana, Stekić, Anđela, Bolland, Samuel J., Jasnić, Nebojša, Ninković, Milica, Zarić Kontić, Marina, Ilić, Tihomir V., Rodger, Jennifer, Nedeljković, Nadežda, Dragić, Milorad, "Intermittent Theta Burst Stimulation Improves Motor and Behavioral Dysfunction through Modulation of NMDA Receptor Subunit Composition in Experimental Model of Parkinson’s Disease" in Cells, 12, no. 11 (2023),
https://doi.org/10.3390/cells12111525 . .

TY  - JOUR
AU  - Đurašević, Siniša
AU  - Ružičić, Aleksandra
AU  - Lakić, Iva
AU  - Tosti, Tomislav
AU  - Đurović, Saša
AU  - Glumac, Sofija
AU  - Pejić, Snežana
AU  - Todorović, Ana
AU  - Drakulić, Dunja R.
AU  - Stanković, Sanja
AU  - Jasnić, Nebojša
AU  - Đorđević, Jelena
AU  - Todorović, Zoran
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10173
AB  - A dysregulated and overwhelming response to an infection accompanied by the exaggerated pro-inflammatory state and metabolism disturbance leads to the fatal outcome in sepsis. Previously we showed that meldonium, an anti-ischemic drug clinically used to treat myocardial and cerebral ischemia, strongly increases mortality in faecal-induced peritonitis (FIP) in rats. We postulated that the same mechanism that is responsible for the otherwise strong anti-inflammatory effects of meldonium could be the culprit of the increased mortality. In the present study, we applied the LPS-induced model of sepsis to explore the presence of any differences from and/or similarities to the FIP model. When it comes to energy production, despite some shared similarities, it is evident that LPS and FIP models of sepsis differ greatly. A different profile of sympathoadrenal activation may account for this observation, as it was lacking in the FIP model, whereas in the LPS model it was strong enough to overcome the effects of meldonium. Therefore, choosing the appropriate model of sepsis induction is of great importance, especially if energy homeostasis is the main focus of the study. Even when differences in the experimental design of the two models are acknowledged, the role of different patterns of energy production cannot be excluded. On that account, our results draw attention to the importance of uninterrupted energy production in sepsis but also call for much-needed revisions of the current recommendations for its treatment.
T2  - International Journal of Molecular Sciences
T1  - The Effects of a Meldonium Pre-Treatment on the Course of the LPS-Induced Sepsis in Rats
VL  - 23
IS  - 4
SP  - 2395
DO  - 10.3390/ijms23042395
ER  - 

@article{
author = "Đurašević, Siniša and Ružičić, Aleksandra and Lakić, Iva and Tosti, Tomislav and Đurović, Saša and Glumac, Sofija and Pejić, Snežana and Todorović, Ana and Drakulić, Dunja R. and Stanković, Sanja and Jasnić, Nebojša and Đorđević, Jelena and Todorović, Zoran",
year = "2022",
abstract = "A dysregulated and overwhelming response to an infection accompanied by the exaggerated pro-inflammatory state and metabolism disturbance leads to the fatal outcome in sepsis. Previously we showed that meldonium, an anti-ischemic drug clinically used to treat myocardial and cerebral ischemia, strongly increases mortality in faecal-induced peritonitis (FIP) in rats. We postulated that the same mechanism that is responsible for the otherwise strong anti-inflammatory effects of meldonium could be the culprit of the increased mortality. In the present study, we applied the LPS-induced model of sepsis to explore the presence of any differences from and/or similarities to the FIP model. When it comes to energy production, despite some shared similarities, it is evident that LPS and FIP models of sepsis differ greatly. A different profile of sympathoadrenal activation may account for this observation, as it was lacking in the FIP model, whereas in the LPS model it was strong enough to overcome the effects of meldonium. Therefore, choosing the appropriate model of sepsis induction is of great importance, especially if energy homeostasis is the main focus of the study. Even when differences in the experimental design of the two models are acknowledged, the role of different patterns of energy production cannot be excluded. On that account, our results draw attention to the importance of uninterrupted energy production in sepsis but also call for much-needed revisions of the current recommendations for its treatment.",
journal = "International Journal of Molecular Sciences",
title = "The Effects of a Meldonium Pre-Treatment on the Course of the LPS-Induced Sepsis in Rats",
volume = "23",
number = "4",
pages = "2395",
doi = "10.3390/ijms23042395"
}

Đurašević, S., Ružičić, A., Lakić, I., Tosti, T., Đurović, S., Glumac, S., Pejić, S., Todorović, A., Drakulić, D. R., Stanković, S., Jasnić, N., Đorđević, J.,& Todorović, Z.. (2022). The Effects of a Meldonium Pre-Treatment on the Course of the LPS-Induced Sepsis in Rats. in International Journal of Molecular Sciences, 23(4), 2395.
https://doi.org/10.3390/ijms23042395

Đurašević S, Ružičić A, Lakić I, Tosti T, Đurović S, Glumac S, Pejić S, Todorović A, Drakulić DR, Stanković S, Jasnić N, Đorđević J, Todorović Z. The Effects of a Meldonium Pre-Treatment on the Course of the LPS-Induced Sepsis in Rats. in International Journal of Molecular Sciences. 2022;23(4):2395.
doi:10.3390/ijms23042395 .

Đurašević, Siniša, Ružičić, Aleksandra, Lakić, Iva, Tosti, Tomislav, Đurović, Saša, Glumac, Sofija, Pejić, Snežana, Todorović, Ana, Drakulić, Dunja R., Stanković, Sanja, Jasnić, Nebojša, Đorđević, Jelena, Todorović, Zoran, "The Effects of a Meldonium Pre-Treatment on the Course of the LPS-Induced Sepsis in Rats" in International Journal of Molecular Sciences, 23, no. 4 (2022):2395,
https://doi.org/10.3390/ijms23042395 . .

TY  - JOUR
AU  - Đurašević, Siniša
AU  - Nikolić, Gorana V.
AU  - Todorović, Ana
AU  - Drakulić, Dunja R.
AU  - Pejić, Snežana
AU  - Martinović, Vesna
AU  - Mitić-Ćulafić, Dragana
AU  - Milić, Dragana
AU  - Kop, Tatjana
AU  - Jasnić, Nebojša
AU  - Đorđević, Jelena D.
AU  - Todorović, Zoran
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8924
AB  - The effects of twelve weeks of supplementation with fullerene C60 olive/coconut oil solution on a broad spectrum of parameters in rats were examined. The tissue bioaccumulation of C60 was shown to be tissue-specific, with the liver, heart, and adrenal glands being the organs of the greatest, and the kidney, brain, and spleen being the organs of the smallest accumulation. C60 did not change aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase serum activities level, nor the damage of liver cells DNA. There were no effects of fullerene on prooxidant-antioxidant balance in the liver, kidney, spleen, heart, and brain, nor any visible harmful effects on the liver, heart, aorta, spleen, kidney, and small intestine histology. Fullerene changed the gut microbiota structure towards the bacteria that ameliorate lipid homeostasis, causing a serum triglycerides concentration decrease. However, C60 significantly increased the insulin resistance, serum ascorbate oxidation, and brain malondialdehyde and advanced oxidation protein products level. The deteriorative effects of C60 on the brain and serum could be attributed to the specific physicochemical composition of these tissues, potentiating the C60 aggregation or biotransformation as the key element of its pro-oxidative action.
T2  - Food and Chemical Toxicology
T1  - Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats
VL  - 140
DO  - 10.1016/j.fct.2020.111302
ER  - 

@article{
author = "Đurašević, Siniša and Nikolić, Gorana V. and Todorović, Ana and Drakulić, Dunja R. and Pejić, Snežana and Martinović, Vesna and Mitić-Ćulafić, Dragana and Milić, Dragana and Kop, Tatjana and Jasnić, Nebojša and Đorđević, Jelena D. and Todorović, Zoran",
year = "2020",
abstract = "The effects of twelve weeks of supplementation with fullerene C60 olive/coconut oil solution on a broad spectrum of parameters in rats were examined. The tissue bioaccumulation of C60 was shown to be tissue-specific, with the liver, heart, and adrenal glands being the organs of the greatest, and the kidney, brain, and spleen being the organs of the smallest accumulation. C60 did not change aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase serum activities level, nor the damage of liver cells DNA. There were no effects of fullerene on prooxidant-antioxidant balance in the liver, kidney, spleen, heart, and brain, nor any visible harmful effects on the liver, heart, aorta, spleen, kidney, and small intestine histology. Fullerene changed the gut microbiota structure towards the bacteria that ameliorate lipid homeostasis, causing a serum triglycerides concentration decrease. However, C60 significantly increased the insulin resistance, serum ascorbate oxidation, and brain malondialdehyde and advanced oxidation protein products level. The deteriorative effects of C60 on the brain and serum could be attributed to the specific physicochemical composition of these tissues, potentiating the C60 aggregation or biotransformation as the key element of its pro-oxidative action.",
journal = "Food and Chemical Toxicology",
title = "Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats",
volume = "140",
doi = "10.1016/j.fct.2020.111302"
}

Đurašević, S., Nikolić, G. V., Todorović, A., Drakulić, D. R., Pejić, S., Martinović, V., Mitić-Ćulafić, D., Milić, D., Kop, T., Jasnić, N., Đorđević, J. D.,& Todorović, Z.. (2020). Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats. in Food and Chemical Toxicology, 140.
https://doi.org/10.1016/j.fct.2020.111302

Đurašević S, Nikolić GV, Todorović A, Drakulić DR, Pejić S, Martinović V, Mitić-Ćulafić D, Milić D, Kop T, Jasnić N, Đorđević JD, Todorović Z. Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats. in Food and Chemical Toxicology. 2020;140.
doi:10.1016/j.fct.2020.111302 .

Đurašević, Siniša, Nikolić, Gorana V., Todorović, Ana, Drakulić, Dunja R., Pejić, Snežana, Martinović, Vesna, Mitić-Ćulafić, Dragana, Milić, Dragana, Kop, Tatjana, Jasnić, Nebojša, Đorđević, Jelena D., Todorović, Zoran, "Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats" in Food and Chemical Toxicology, 140 (2020),
https://doi.org/10.1016/j.fct.2020.111302 . .

TY  - JOUR
AU  - Zafirović, Sonja
AU  - Sudar-Milovanović, Emina
AU  - Obradović, Milan M.
AU  - Đorđević, Jelena D.
AU  - Jasnić, Nebojša
AU  - Labudović-Borović, Milica
AU  - Isenović, Esma R.
PY  - 2019
UR  - http://www.eurekaselect.com/159734/article
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8097
AB  - BACKGROUND: Oestradiol is an important regulatory factor with several positive effects on the cardiovascular (CV) system. We evaluated the molecular mechanism of the in vivo effects of oestradiol on the regulation of cardiac inducible nitric oxide (NO) synthase (iNOS) expression and activity. METHODS: Male Wistar rats were treated with oestradiol (40 mg/kg, intraperitoneally) and after 24 h the animals were sacrificed. The concentrations of NO and L-Arginine (L-Arg) were determined spectrophotometrically. For protein expressions of iNOS, p65 subunit of nuclear factor-κB (NFκB-p65), Ras homolog gene family-member A (RhoA), angiotensin II receptor type 1 (AT1R), insulin receptor substrate 1 (IRS-1), p85, p110 and protein kinase B (Akt), Western blot method was used. Coimmunoprecipitation was used for measuring the association of IRS-1 with the p85 subunit of phosphatidylinositol- 3-kinase (PI3K). The expression of iNOS messenger ribonucleic acid (mRNA) was measured with the quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical analysis of the tissue was used to detect localization and expression of iNOS in heart tissue. RESULTS: Oestradiol treatment reduced L-Arg concentration (p<0.01), iNOS mRNA (p<0.01) and protein (p<0.001) expression, level of RhoA (p<0.05) and AT1R (p<0.001) protein. In contrast, plasma NO (p<0.05), Akt phosphorylation at Thr308 (p<0.05) and protein level of p85 (p<0.001) increased after oestradiol treatment. CONCLUSION: Our results suggest that oestradiol in vivo regulates cardiac iNOS expression via the PI3K/Akt signaling pathway, through attenuation of RhoA and AT1R.
T2  - Current Vascular Pharmacology
T1  - Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression
VL  - 17
IS  - 3
SP  - 307
EP  - 318
DO  - 10.2174/1570161116666180212142414
ER  - 

@article{
author = "Zafirović, Sonja and Sudar-Milovanović, Emina and Obradović, Milan M. and Đorđević, Jelena D. and Jasnić, Nebojša and Labudović-Borović, Milica and Isenović, Esma R.",
year = "2019",
abstract = "BACKGROUND: Oestradiol is an important regulatory factor with several positive effects on the cardiovascular (CV) system. We evaluated the molecular mechanism of the in vivo effects of oestradiol on the regulation of cardiac inducible nitric oxide (NO) synthase (iNOS) expression and activity. METHODS: Male Wistar rats were treated with oestradiol (40 mg/kg, intraperitoneally) and after 24 h the animals were sacrificed. The concentrations of NO and L-Arginine (L-Arg) were determined spectrophotometrically. For protein expressions of iNOS, p65 subunit of nuclear factor-κB (NFκB-p65), Ras homolog gene family-member A (RhoA), angiotensin II receptor type 1 (AT1R), insulin receptor substrate 1 (IRS-1), p85, p110 and protein kinase B (Akt), Western blot method was used. Coimmunoprecipitation was used for measuring the association of IRS-1 with the p85 subunit of phosphatidylinositol- 3-kinase (PI3K). The expression of iNOS messenger ribonucleic acid (mRNA) was measured with the quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical analysis of the tissue was used to detect localization and expression of iNOS in heart tissue. RESULTS: Oestradiol treatment reduced L-Arg concentration (p<0.01), iNOS mRNA (p<0.01) and protein (p<0.001) expression, level of RhoA (p<0.05) and AT1R (p<0.001) protein. In contrast, plasma NO (p<0.05), Akt phosphorylation at Thr308 (p<0.05) and protein level of p85 (p<0.001) increased after oestradiol treatment. CONCLUSION: Our results suggest that oestradiol in vivo regulates cardiac iNOS expression via the PI3K/Akt signaling pathway, through attenuation of RhoA and AT1R.",
journal = "Current Vascular Pharmacology",
title = "Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression",
volume = "17",
number = "3",
pages = "307-318",
doi = "10.2174/1570161116666180212142414"
}

Zafirović, S., Sudar-Milovanović, E., Obradović, M. M., Đorđević, J. D., Jasnić, N., Labudović-Borović, M.,& Isenović, E. R.. (2019). Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression. in Current Vascular Pharmacology, 17(3), 307-318.
https://doi.org/10.2174/1570161116666180212142414

Zafirović S, Sudar-Milovanović E, Obradović MM, Đorđević JD, Jasnić N, Labudović-Borović M, Isenović ER. Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression. in Current Vascular Pharmacology. 2019;17(3):307-318.
doi:10.2174/1570161116666180212142414 .

Zafirović, Sonja, Sudar-Milovanović, Emina, Obradović, Milan M., Đorđević, Jelena D., Jasnić, Nebojša, Labudović-Borović, Milica, Isenović, Esma R., "Involvement of PI3K, Akt and RhoA in Oestradiol Regulation of Cardiac iNOS Expression" in Current Vascular Pharmacology, 17, no. 3 (2019):307-318,
https://doi.org/10.2174/1570161116666180212142414 . .

TY  - JOUR
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7584
AB  - The dysfunction of parvalbumin-positive (PV+) interneurons, the most abundant type of hippocampal GABAergic inhibitory interneuron, has been implicated in mood disorders. We recently reported that adult male Wistar rats exposed to three weeks of social isolation show depressive-and anxiety-like behaviors and a reduced number of PV+ interneurons in all hippocampal subregions. As GABA neurotransmission has been proposed as a potential therapeutic target of antidepressant and antipsychotic medications, we examined whether treatment with the antidepressant fluoxetine (Flx) (15 mg/kg/day) or the antipsychotic clozapine (Clz) (20 mg/kg/day) during three weeks of social isolation in rats offered protection from the isolation stress-induced reduction in the number of PV+ interneurons in hippocampal subregions. Using immunofluorescence analysis, we revealed that both chronic Flx and Clz partially prevented the isolation-induced changes. Flx prevented the reduction in the number of PV+ interneurons in the CA2, CA3, without affecting the CA1 and dentate gyrus DG areas, whereas Clz prevented this decrement in the CA2, CA3 and DG regions but not in CA1 areas. Moreover, Flx increased the number of PV+ interneurons in CA1 in control animals. These findings suggest that chronic administration of Flx or Clz may offer partial protection from social isolation stress via modulation of the hippocampal GABAergic system. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
T2  - Neuroscience
T1  - Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus
VL  - 371
SP  - 384
EP  - 394
DO  - 10.1016/j.neuroscience.2017.12.020
ER  - 

@article{
year = "2018",
abstract = "The dysfunction of parvalbumin-positive (PV+) interneurons, the most abundant type of hippocampal GABAergic inhibitory interneuron, has been implicated in mood disorders. We recently reported that adult male Wistar rats exposed to three weeks of social isolation show depressive-and anxiety-like behaviors and a reduced number of PV+ interneurons in all hippocampal subregions. As GABA neurotransmission has been proposed as a potential therapeutic target of antidepressant and antipsychotic medications, we examined whether treatment with the antidepressant fluoxetine (Flx) (15 mg/kg/day) or the antipsychotic clozapine (Clz) (20 mg/kg/day) during three weeks of social isolation in rats offered protection from the isolation stress-induced reduction in the number of PV+ interneurons in hippocampal subregions. Using immunofluorescence analysis, we revealed that both chronic Flx and Clz partially prevented the isolation-induced changes. Flx prevented the reduction in the number of PV+ interneurons in the CA2, CA3, without affecting the CA1 and dentate gyrus DG areas, whereas Clz prevented this decrement in the CA2, CA3 and DG regions but not in CA1 areas. Moreover, Flx increased the number of PV+ interneurons in CA1 in control animals. These findings suggest that chronic administration of Flx or Clz may offer partial protection from social isolation stress via modulation of the hippocampal GABAergic system. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.",
journal = "Neuroscience",
title = "Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus",
volume = "371",
pages = "384-394",
doi = "10.1016/j.neuroscience.2017.12.020"
}

(2018). Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus. in Neuroscience, 371, 384-394.
https://doi.org/10.1016/j.neuroscience.2017.12.020

Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus. in Neuroscience. 2018;371:384-394.
doi:10.1016/j.neuroscience.2017.12.020 .

"Chronic Treatment with Fluoxetine or Clozapine of Socially Isolated Rats Prevents Subsector-Specific Reduction of Parvalbumin Immunoreactive Cells in the Hippocampus" in Neuroscience, 371 (2018):384-394,
https://doi.org/10.1016/j.neuroscience.2017.12.020 . .

TY  - JOUR
AU  - Stefanović, Bojana
AU  - Spasojević, Nataša
AU  - Jovanović, Predrag
AU  - Jasnić, Nebojša
AU  - Đorđević, Jelena D.
AU  - Dronjak, Slađana
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1265
AB  - The hippocampus is sensitive to stress which activates norepinephrine terminals deriving from the locus coeruleus. Melatonin exerts positive effects on the hippocampal neurogenic process and on depressive-like behaviour. Thus, in the present study, an examination was made of the effect of chronic melatonin treatment on norepinephrine content, synthesis, uptake, vesicular transport and degradation in the hippocampus of rats exposed to CUMS. This entailed quantifying the norephinephrine, mRNA and protein levels of DBH, NET, VMAT 2, MAO-A and COMT. The results show that CUMS evoked prolonged immobility. Melatonin treatment decreased immobility in comparison with the placebo group, reflecting an antidepressant-like effect. Compared with the placebo group, a dramatic decrease in norepinephrine content, decreased VMAT2 mRNA and protein and increased MAO-A protein levels in the hippocampus of the CUMS rats were observed. However, no significant differences in the levels of DBH, NET, COMT mRNA and protein and MAO-A mRNA levels between the placebo and the stressed groups were found. The results showed the restorative effects of melatonin on the stress-induced decline in the norepinephrine content of the hippocampus. It was observed that melatonin treatment in the CUMS rats prevented the stress-induced decrease in VMAT2 mRNA and protein levels, whereas it reduced the increase of the mRNA of COMT and protein levels of MAO-A. Chronic treatment with melatonin failed to alter the gene expression of DBH or NET in the hippocampus of the CUMS rats. Additionally, the results show that melatonin enhances VMAT2 expression and norepinephrine storage, whilst it reduces norepinephrine degrading enzymes. (C) 2016 Elsevier B.V. and ECNP. All rights reserved.
T2  - European Neuropsychopharmacology
T1  - Melatonin mediated antidepressant-like effect in the hippocampus of chronic stress-induced depression rats: Regulating vesicular monoamine transporter 2 and monoamine oxidase A levels
VL  - 26
IS  - 10
SP  - 1629
EP  - 1637
DO  - 10.1016/j.euroneuro.2016.07.005
ER  - 

@article{
author = "Stefanović, Bojana and Spasojević, Nataša and Jovanović, Predrag and Jasnić, Nebojša and Đorđević, Jelena D. and Dronjak, Slađana",
year = "2016",
abstract = "The hippocampus is sensitive to stress which activates norepinephrine terminals deriving from the locus coeruleus. Melatonin exerts positive effects on the hippocampal neurogenic process and on depressive-like behaviour. Thus, in the present study, an examination was made of the effect of chronic melatonin treatment on norepinephrine content, synthesis, uptake, vesicular transport and degradation in the hippocampus of rats exposed to CUMS. This entailed quantifying the norephinephrine, mRNA and protein levels of DBH, NET, VMAT 2, MAO-A and COMT. The results show that CUMS evoked prolonged immobility. Melatonin treatment decreased immobility in comparison with the placebo group, reflecting an antidepressant-like effect. Compared with the placebo group, a dramatic decrease in norepinephrine content, decreased VMAT2 mRNA and protein and increased MAO-A protein levels in the hippocampus of the CUMS rats were observed. However, no significant differences in the levels of DBH, NET, COMT mRNA and protein and MAO-A mRNA levels between the placebo and the stressed groups were found. The results showed the restorative effects of melatonin on the stress-induced decline in the norepinephrine content of the hippocampus. It was observed that melatonin treatment in the CUMS rats prevented the stress-induced decrease in VMAT2 mRNA and protein levels, whereas it reduced the increase of the mRNA of COMT and protein levels of MAO-A. Chronic treatment with melatonin failed to alter the gene expression of DBH or NET in the hippocampus of the CUMS rats. Additionally, the results show that melatonin enhances VMAT2 expression and norepinephrine storage, whilst it reduces norepinephrine degrading enzymes. (C) 2016 Elsevier B.V. and ECNP. All rights reserved.",
journal = "European Neuropsychopharmacology",
title = "Melatonin mediated antidepressant-like effect in the hippocampus of chronic stress-induced depression rats: Regulating vesicular monoamine transporter 2 and monoamine oxidase A levels",
volume = "26",
number = "10",
pages = "1629-1637",
doi = "10.1016/j.euroneuro.2016.07.005"
}

Stefanović, B., Spasojević, N., Jovanović, P., Jasnić, N., Đorđević, J. D.,& Dronjak, S.. (2016). Melatonin mediated antidepressant-like effect in the hippocampus of chronic stress-induced depression rats: Regulating vesicular monoamine transporter 2 and monoamine oxidase A levels. in European Neuropsychopharmacology, 26(10), 1629-1637.
https://doi.org/10.1016/j.euroneuro.2016.07.005

Stefanović B, Spasojević N, Jovanović P, Jasnić N, Đorđević JD, Dronjak S. Melatonin mediated antidepressant-like effect in the hippocampus of chronic stress-induced depression rats: Regulating vesicular monoamine transporter 2 and monoamine oxidase A levels. in European Neuropsychopharmacology. 2016;26(10):1629-1637.
doi:10.1016/j.euroneuro.2016.07.005 .

Stefanović, Bojana, Spasojević, Nataša, Jovanović, Predrag, Jasnić, Nebojša, Đorđević, Jelena D., Dronjak, Slađana, "Melatonin mediated antidepressant-like effect in the hippocampus of chronic stress-induced depression rats: Regulating vesicular monoamine transporter 2 and monoamine oxidase A levels" in European Neuropsychopharmacology, 26, no. 10 (2016):1629-1637,
https://doi.org/10.1016/j.euroneuro.2016.07.005 . .

TY  - JOUR
AU  - Vujović, Predrag
AU  - Lakić, Iva
AU  - Jasnić, Nebojša
AU  - Jevđović, Tanja
AU  - Đurašević, Siniša F.
AU  - Isenović, Esma R.
AU  - Đorđević, Jelena
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1120
AB  - Given that both prolactin and galanin take part in the regulation of energy homeostasis and that galanin is localized within lactotrophs, this study was aimed at comparing the pituitary expression patterns of prolactin and galanin during different phases of metabolic response to starvation in adult Wistar male rats. Food was removed at the onset of the dark phase (6:00 pm) and the animals were deprived for 6, 12, 24 and 48 h. Each of the starved groups (n=6) was killed simultaneously with a group of ad libitum-fed rats (n=6), and the intrapituitary levels of prolactin and galanin were examined. Galanin expression in the hypothalamus and the circulating levels of prolactin were also assessed. Starvation induced a rise in the intrapituitary prolactin level (p LT 0.001), whereas the opposite trend was detected in the serum (p LT 0.05). The galanin pituitary level was initially increased (6, 12 h) (p LT 0.05), but as starvation progressed, it first reached (at 24 h) and ultimately fell below the level recorded in the ad libitum rats (at 48 h) (p LT 0.05). Both prolactin and galanin were elevated in the hypothalamus after 24- and 48-h starvation. The results show that the starvation-induced increase in the pituitary prolactin expression did not lead to the rise in prolactin circulating levels, but rather resulted in the elevation of the prolactin hypothalamic content. Furthermore, the results suggest that under the circumstances of disturbed energy homeostasis, galanin might be responsible for the augmented prolactin production, initially at the pituitary and subsequently at the hypothalamic level.
T2  - Archives of Biological Sciences
T1  - Time-Dependent Effects of Starvation on Pituitary, Hypothalamic and Serum Prolactin Levels in Rats: Comparison to the Galanin Expression Pattern
VL  - 68
IS  - 1
SP  - 117
EP  - 123
DO  - 10.2298/ABS150525133V
ER  - 

@article{
author = "Vujović, Predrag and Lakić, Iva and Jasnić, Nebojša and Jevđović, Tanja and Đurašević, Siniša F. and Isenović, Esma R. and Đorđević, Jelena",
year = "2016",
abstract = "Given that both prolactin and galanin take part in the regulation of energy homeostasis and that galanin is localized within lactotrophs, this study was aimed at comparing the pituitary expression patterns of prolactin and galanin during different phases of metabolic response to starvation in adult Wistar male rats. Food was removed at the onset of the dark phase (6:00 pm) and the animals were deprived for 6, 12, 24 and 48 h. Each of the starved groups (n=6) was killed simultaneously with a group of ad libitum-fed rats (n=6), and the intrapituitary levels of prolactin and galanin were examined. Galanin expression in the hypothalamus and the circulating levels of prolactin were also assessed. Starvation induced a rise in the intrapituitary prolactin level (p LT 0.001), whereas the opposite trend was detected in the serum (p LT 0.05). The galanin pituitary level was initially increased (6, 12 h) (p LT 0.05), but as starvation progressed, it first reached (at 24 h) and ultimately fell below the level recorded in the ad libitum rats (at 48 h) (p LT 0.05). Both prolactin and galanin were elevated in the hypothalamus after 24- and 48-h starvation. The results show that the starvation-induced increase in the pituitary prolactin expression did not lead to the rise in prolactin circulating levels, but rather resulted in the elevation of the prolactin hypothalamic content. Furthermore, the results suggest that under the circumstances of disturbed energy homeostasis, galanin might be responsible for the augmented prolactin production, initially at the pituitary and subsequently at the hypothalamic level.",
journal = "Archives of Biological Sciences",
title = "Time-Dependent Effects of Starvation on Pituitary, Hypothalamic and Serum Prolactin Levels in Rats: Comparison to the Galanin Expression Pattern",
volume = "68",
number = "1",
pages = "117-123",
doi = "10.2298/ABS150525133V"
}

Vujović, P., Lakić, I., Jasnić, N., Jevđović, T., Đurašević, S. F., Isenović, E. R.,& Đorđević, J.. (2016). Time-Dependent Effects of Starvation on Pituitary, Hypothalamic and Serum Prolactin Levels in Rats: Comparison to the Galanin Expression Pattern. in Archives of Biological Sciences, 68(1), 117-123.
https://doi.org/10.2298/ABS150525133V

Vujović P, Lakić I, Jasnić N, Jevđović T, Đurašević SF, Isenović ER, Đorđević J. Time-Dependent Effects of Starvation on Pituitary, Hypothalamic and Serum Prolactin Levels in Rats: Comparison to the Galanin Expression Pattern. in Archives of Biological Sciences. 2016;68(1):117-123.
doi:10.2298/ABS150525133V .

Vujović, Predrag, Lakić, Iva, Jasnić, Nebojša, Jevđović, Tanja, Đurašević, Siniša F., Isenović, Esma R., Đorđević, Jelena, "Time-Dependent Effects of Starvation on Pituitary, Hypothalamic and Serum Prolactin Levels in Rats: Comparison to the Galanin Expression Pattern" in Archives of Biological Sciences, 68, no. 1 (2016):117-123,
https://doi.org/10.2298/ABS150525133V . .

TY  - JOUR
AU  - Bogdanović, Nikola
AU  - Obradović, Milan M.
AU  - Jasnić, Nebojša
AU  - Spremo-Potparević, Biljana
AU  - Unić-Stojanović, Dragana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10318
AB  - Prema podacima Svetske zdravstvene organizacije, 15 miliona ljudi godišnje doživi moždani udar. Najčešći uzročnik moždanog udara je ishemija mozga, koja se dešava u skoro 85% slučajeva. Moždana ishemija izazvana tromboembolijskim događajima definiše se kao trajno ili prolazno smanjenje cirkulacije krvi, što za posledicu ima nedostatak kiseonika, glukoze i ostalih važnih nutritijenata, dovodeći postepeno do metaboličkih promena i apoptoze ćelija. Tokom operativnih zahvata kao što je karotidna endarterektomija (CEA) može doći do hipoksično-ishemičnog stanja mozga ili akutne ishemije mozga (ABI), kao i do samog moždanog udara. Glavni uzrok ABI u toku CEA je cerebralna hipoperfuzija koja je uzrokovana klemovanjem karotidne arterije, pri čemu dolazi do hipoksije, što može predstavljati jedan od okidača za niz fizioloških odgovora organizma, među kojima je oslobađanje različitih medijatora inflamacije. Jedan od medijatora inflamacije je i azot monoksid (NO), slobodni radikal koji pored mnogobrojnih fizioloških efekata ima važnu ulogu i u samom imunom odgovoru organizma. Međutim, NO može biti veoma štetan i svojim delovanjem dovesti do oštećenja ćelija i tkiva. Nedostatak podataka u literaturi o ulozi endotelne NOS (eNOS) i inducibilne NOS (iNOS) tokom CEA, kao i mehanizama njihove regulacije u stanjima ishemije, ukazuju na pravac kojim treba da se usmere buduća istraživanja. Poznavanje molekularnih mehanizama regulacije aktivnosti i ekspresije iNOS, svakako će pomoći razvoju novih terapijskih strategija u tretmanu štetnih efekata produkcije slobodnih radikala, pre svega nekontrolisane produkcije NO.
AB  - According to the World Health Organization, 15 million people per year are affected by stroke. The most common cause of stroke is brain ischemia, which occurs in almost 85% of cases. Ischemia caused by thromboembolism is defined as permanently or temporarily decreased blood flow which prevents an adequate delivery of oxygen, glucose and other important nutrients, leading progressively to metabolic changes and cell apoptosis. Carotid endarterectomy (CEA) can cause hypoxic - ischemic states of the brain or acute brain ischemia (ABI) leading eventually to stroke. The main cause of ABI as a result of CEA is cerebral hypoperfusion caused by clamping of carotid arteries, when hypoxia occurs.. Hypoxia per se is one of the triggers of complex physiological responses in the body, including the release of various mediators of inflammation. One of these inflammatory mediators is nitric oxide (NO), a free radical which has numerous physiological effects and also plays an important role in the immune response of the organism. However, NO may be very harmful and cause cell and tissue damage. The lack of literature data on the role of endothelial NOS (eNOS) and inducible NOS (iNOS) during CEA, as well as the mechanisms of their regulation in ischemic conditions, suggest that intensifying future research in this field is very important. An insight into molecular mechanisms of iNOS activity and expression regulation will certainly help to develop new therapeutic strategies for treating harmful effects of free radicals, especially uncontrolled production of NO.
T2  - Medicinska istraživanja
T1  - Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije
T1  - The role of the nitric oxide synthases in brain ischemia during carotid endarterectomy
VL  - 49
IS  - 1
SP  - 40
EP  - 46
DO  - 10.5937/MedIst1501040B
ER  - 

@article{
author = "Bogdanović, Nikola and Obradović, Milan M. and Jasnić, Nebojša and Spremo-Potparević, Biljana and Unić-Stojanović, Dragana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2015",
abstract = "Prema podacima Svetske zdravstvene organizacije, 15 miliona ljudi godišnje doživi moždani udar. Najčešći uzročnik moždanog udara je ishemija mozga, koja se dešava u skoro 85% slučajeva. Moždana ishemija izazvana tromboembolijskim događajima definiše se kao trajno ili prolazno smanjenje cirkulacije krvi, što za posledicu ima nedostatak kiseonika, glukoze i ostalih važnih nutritijenata, dovodeći postepeno do metaboličkih promena i apoptoze ćelija. Tokom operativnih zahvata kao što je karotidna endarterektomija (CEA) može doći do hipoksično-ishemičnog stanja mozga ili akutne ishemije mozga (ABI), kao i do samog moždanog udara. Glavni uzrok ABI u toku CEA je cerebralna hipoperfuzija koja je uzrokovana klemovanjem karotidne arterije, pri čemu dolazi do hipoksije, što može predstavljati jedan od okidača za niz fizioloških odgovora organizma, među kojima je oslobađanje različitih medijatora inflamacije. Jedan od medijatora inflamacije je i azot monoksid (NO), slobodni radikal koji pored mnogobrojnih fizioloških efekata ima važnu ulogu i u samom imunom odgovoru organizma. Međutim, NO može biti veoma štetan i svojim delovanjem dovesti do oštećenja ćelija i tkiva. Nedostatak podataka u literaturi o ulozi endotelne NOS (eNOS) i inducibilne NOS (iNOS) tokom CEA, kao i mehanizama njihove regulacije u stanjima ishemije, ukazuju na pravac kojim treba da se usmere buduća istraživanja. Poznavanje molekularnih mehanizama regulacije aktivnosti i ekspresije iNOS, svakako će pomoći razvoju novih terapijskih strategija u tretmanu štetnih efekata produkcije slobodnih radikala, pre svega nekontrolisane produkcije NO., According to the World Health Organization, 15 million people per year are affected by stroke. The most common cause of stroke is brain ischemia, which occurs in almost 85% of cases. Ischemia caused by thromboembolism is defined as permanently or temporarily decreased blood flow which prevents an adequate delivery of oxygen, glucose and other important nutrients, leading progressively to metabolic changes and cell apoptosis. Carotid endarterectomy (CEA) can cause hypoxic - ischemic states of the brain or acute brain ischemia (ABI) leading eventually to stroke. The main cause of ABI as a result of CEA is cerebral hypoperfusion caused by clamping of carotid arteries, when hypoxia occurs.. Hypoxia per se is one of the triggers of complex physiological responses in the body, including the release of various mediators of inflammation. One of these inflammatory mediators is nitric oxide (NO), a free radical which has numerous physiological effects and also plays an important role in the immune response of the organism. However, NO may be very harmful and cause cell and tissue damage. The lack of literature data on the role of endothelial NOS (eNOS) and inducible NOS (iNOS) during CEA, as well as the mechanisms of their regulation in ischemic conditions, suggest that intensifying future research in this field is very important. An insight into molecular mechanisms of iNOS activity and expression regulation will certainly help to develop new therapeutic strategies for treating harmful effects of free radicals, especially uncontrolled production of NO.",
journal = "Medicinska istraživanja",
title = "Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije, The role of the nitric oxide synthases in brain ischemia during carotid endarterectomy",
volume = "49",
number = "1",
pages = "40-46",
doi = "10.5937/MedIst1501040B"
}

Bogdanović, N., Obradović, M. M., Jasnić, N., Spremo-Potparević, B., Unić-Stojanović, D., Radak, Đ. J.,& Isenović, E. R.. (2015). Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije. in Medicinska istraživanja, 49(1), 40-46.
https://doi.org/10.5937/MedIst1501040B

Bogdanović N, Obradović MM, Jasnić N, Spremo-Potparević B, Unić-Stojanović D, Radak ĐJ, Isenović ER. Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije. in Medicinska istraživanja. 2015;49(1):40-46.
doi:10.5937/MedIst1501040B .

Bogdanović, Nikola, Obradović, Milan M., Jasnić, Nebojša, Spremo-Potparević, Biljana, Unić-Stojanović, Dragana, Radak, Đorđe J., Isenović, Esma R., "Uloga azot-monoksid sintaza u stanjima ishemije mozga tokom karotidne endarterektomije" in Medicinska istraživanja, 49, no. 1 (2015):40-46,
https://doi.org/10.5937/MedIst1501040B . .