Petrović, Zorica

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  • Petrović, Zorica (2)
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Protective effects of whey on rat liver damage induced by chronic alcohol intake

Radić, Ivan; Mijović, Milica; Tatalović, Nikola R.; Mitić, Miloš; Lukić, Vera; Joksimović, Bojan; Petrović, Zorica; Ristić, Siniša; Veličković, Stefan; Nestorović, Vojkan; Ćorac, Aleksandar M.; Mirić, Mirjana; Adžić, Miroslav; Blagojević, Duško P.; Popović, Ljiljana M.; Janićijević-Hudomal, Snežana

(2019)

TY  - JOUR
AU  - Radić, Ivan
AU  - Mijović, Milica
AU  - Tatalović, Nikola R.
AU  - Mitić, Miloš
AU  - Lukić, Vera
AU  - Joksimović, Bojan
AU  - Petrović, Zorica
AU  - Ristić, Siniša
AU  - Veličković, Stefan
AU  - Nestorović, Vojkan
AU  - Ćorac, Aleksandar M.
AU  - Mirić, Mirjana
AU  - Adžić, Miroslav
AU  - Blagojević, Duško P.
AU  - Popović, Ljiljana M.
AU  - Janićijević-Hudomal, Snežana
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8541
AB  - In 2012, alcohol liver disease resulted in 3.3 million—5.9% of global deaths. This study introduced whey protection capacity against chronic alcohol-induced liver injury. Rats were orally administered to 12% ethanol solution in water (ad libitum, average 8.14 g of ethanol/kg body weight (b.w.)/day) alone or combined with whey (per os, 2 g/kg b.w./day). After 6-week treatment, chronic ethanol consumption induced significant histopathological liver changes: congestion, central vein dilation, hepatic portal vein branch dilation, Kupffer cells hyperplasia, fatty liver changes, and hepatocytes focal necrosis. Ethanol significantly increased liver catalase activity and glutathione reductase protein expression without significant effects on antioxidative enzymes: glutathione peroxidase (GPx), copper–zinc-containing superoxide dismutase (CuZnSOD) and manganese-containing superoxide dismutase (MnSOD). Co-treatment with whey significantly attenuated pathohistological changes induced by ethanol ingestion and increased GSH-Px and nuclear factor kappa B (NF-κB) protein expression. Our results showed positive effects of whey on liver chronically exposed to ethanol, which seem to be associated with NF-κB-GPx signaling. © The Author(s) 2019.
T2  - Human & Experimental Toxicology
T1  - Protective effects of whey on rat liver damage induced by chronic alcohol intake
VL  - 38
IS  - 6
SP  - 632
EP  - 645
DO  - 10.1177/0960327119829518
ER  - 
@article{
author = "Radić, Ivan and Mijović, Milica and Tatalović, Nikola R. and Mitić, Miloš and Lukić, Vera and Joksimović, Bojan and Petrović, Zorica and Ristić, Siniša and Veličković, Stefan and Nestorović, Vojkan and Ćorac, Aleksandar M. and Mirić, Mirjana and Adžić, Miroslav and Blagojević, Duško P. and Popović, Ljiljana M. and Janićijević-Hudomal, Snežana",
year = "2019",
abstract = "In 2012, alcohol liver disease resulted in 3.3 million—5.9% of global deaths. This study introduced whey protection capacity against chronic alcohol-induced liver injury. Rats were orally administered to 12% ethanol solution in water (ad libitum, average 8.14 g of ethanol/kg body weight (b.w.)/day) alone or combined with whey (per os, 2 g/kg b.w./day). After 6-week treatment, chronic ethanol consumption induced significant histopathological liver changes: congestion, central vein dilation, hepatic portal vein branch dilation, Kupffer cells hyperplasia, fatty liver changes, and hepatocytes focal necrosis. Ethanol significantly increased liver catalase activity and glutathione reductase protein expression without significant effects on antioxidative enzymes: glutathione peroxidase (GPx), copper–zinc-containing superoxide dismutase (CuZnSOD) and manganese-containing superoxide dismutase (MnSOD). Co-treatment with whey significantly attenuated pathohistological changes induced by ethanol ingestion and increased GSH-Px and nuclear factor kappa B (NF-κB) protein expression. Our results showed positive effects of whey on liver chronically exposed to ethanol, which seem to be associated with NF-κB-GPx signaling. © The Author(s) 2019.",
journal = "Human & Experimental Toxicology",
title = "Protective effects of whey on rat liver damage induced by chronic alcohol intake",
volume = "38",
number = "6",
pages = "632-645",
doi = "10.1177/0960327119829518"
}
Radić, I., Mijović, M., Tatalović, N. R., Mitić, M., Lukić, V., Joksimović, B., Petrović, Z., Ristić, S., Veličković, S., Nestorović, V., Ćorac, A. M., Mirić, M., Adžić, M., Blagojević, D. P., Popović, L. M.,& Janićijević-Hudomal, S.. (2019). Protective effects of whey on rat liver damage induced by chronic alcohol intake. in Human & Experimental Toxicology, 38(6), 632-645.
https://doi.org/10.1177/0960327119829518
Radić I, Mijović M, Tatalović NR, Mitić M, Lukić V, Joksimović B, Petrović Z, Ristić S, Veličković S, Nestorović V, Ćorac AM, Mirić M, Adžić M, Blagojević DP, Popović LM, Janićijević-Hudomal S. Protective effects of whey on rat liver damage induced by chronic alcohol intake. in Human & Experimental Toxicology. 2019;38(6):632-645.
doi:10.1177/0960327119829518 .
Radić, Ivan, Mijović, Milica, Tatalović, Nikola R., Mitić, Miloš, Lukić, Vera, Joksimović, Bojan, Petrović, Zorica, Ristić, Siniša, Veličković, Stefan, Nestorović, Vojkan, Ćorac, Aleksandar M., Mirić, Mirjana, Adžić, Miroslav, Blagojević, Duško P., Popović, Ljiljana M., Janićijević-Hudomal, Snežana, "Protective effects of whey on rat liver damage induced by chronic alcohol intake" in Human & Experimental Toxicology, 38, no. 6 (2019):632-645,
https://doi.org/10.1177/0960327119829518 . .
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Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression

Francija, Ester; Petrović, Zorica; Brkić, Željka; Mitić, Miloš; Radulović, Jelena; Adžić, Miroslav

(2019)

TY  - JOUR
AU  - Francija, Ester
AU  - Petrović, Zorica
AU  - Brkić, Željka
AU  - Mitić, Miloš
AU  - Radulović, Jelena
AU  - Adžić, Miroslav
PY  - 2019
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8450
AB  - Recent reports have demonstrated that lipopolysaccharide (LPS)-induced depressive-like behaviour is mediated via NMDA receptor. In this study, we further investigated the role of GluN2 A subunit of NMDA receptor in synaptic processes in the prefrontal cortex (PFC) and hippocampus of GluN2 A knockout (KO) mice in LPS-induced depressive-like behavior. Our data suggest that LPS-treated mice, lacking GluN2 A subunit, did not exhibit depressive-like behaviour. This was accompanied by unaltered levels of IL-6 and significant changes in neuroplasticity markers and glutamate receptor subunits composition in PFC and hippocampus. In particular, an immune challenge in GluN2 A KO mice resulted in unchanged PSA-NCAM levels and proBDNF increase in both brain structures as well as in increase in BDNF levels in hippocampus. Furthermore, the absence of GluN2 A resulted in increased levels of all NCAM isoforms in PFC upon LPS which was followed with a decrease in GluN1 and GluN2B subunits. The levels of AMPA receptor subunits (GluA1, GluA3, and GluA4) in the hippocampus of GluN2 A mice were unaltered upon the treatment and abundantly present in the PFC of KO mice. These results indicate that the GluN2 A subunit is critical in neuroinflammation-related depression, that its absence abolishes LPS-induced depressive phenotype, sustains PSA-NCAM levels, increases proBDNF signalling in the PFC and hippocampus and potentiates synaptic stabilization through NCAM in the PFC upon an immune challenge. © 2018 Elsevier B.V.
T2  - Behavioural Brain Research
T1  - Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression
VL  - 359
SP  - 550
EP  - 559
DO  - 10.1016/j.bbr.2018.10.011
ER  - 
@article{
author = "Francija, Ester and Petrović, Zorica and Brkić, Željka and Mitić, Miloš and Radulović, Jelena and Adžić, Miroslav",
year = "2019",
abstract = "Recent reports have demonstrated that lipopolysaccharide (LPS)-induced depressive-like behaviour is mediated via NMDA receptor. In this study, we further investigated the role of GluN2 A subunit of NMDA receptor in synaptic processes in the prefrontal cortex (PFC) and hippocampus of GluN2 A knockout (KO) mice in LPS-induced depressive-like behavior. Our data suggest that LPS-treated mice, lacking GluN2 A subunit, did not exhibit depressive-like behaviour. This was accompanied by unaltered levels of IL-6 and significant changes in neuroplasticity markers and glutamate receptor subunits composition in PFC and hippocampus. In particular, an immune challenge in GluN2 A KO mice resulted in unchanged PSA-NCAM levels and proBDNF increase in both brain structures as well as in increase in BDNF levels in hippocampus. Furthermore, the absence of GluN2 A resulted in increased levels of all NCAM isoforms in PFC upon LPS which was followed with a decrease in GluN1 and GluN2B subunits. The levels of AMPA receptor subunits (GluA1, GluA3, and GluA4) in the hippocampus of GluN2 A mice were unaltered upon the treatment and abundantly present in the PFC of KO mice. These results indicate that the GluN2 A subunit is critical in neuroinflammation-related depression, that its absence abolishes LPS-induced depressive phenotype, sustains PSA-NCAM levels, increases proBDNF signalling in the PFC and hippocampus and potentiates synaptic stabilization through NCAM in the PFC upon an immune challenge. © 2018 Elsevier B.V.",
journal = "Behavioural Brain Research",
title = "Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression",
volume = "359",
pages = "550-559",
doi = "10.1016/j.bbr.2018.10.011"
}
Francija, E., Petrović, Z., Brkić, Ž., Mitić, M., Radulović, J.,& Adžić, M.. (2019). Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression. in Behavioural Brain Research, 359, 550-559.
https://doi.org/10.1016/j.bbr.2018.10.011
Francija E, Petrović Z, Brkić Ž, Mitić M, Radulović J, Adžić M. Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression. in Behavioural Brain Research. 2019;359:550-559.
doi:10.1016/j.bbr.2018.10.011 .
Francija, Ester, Petrović, Zorica, Brkić, Željka, Mitić, Miloš, Radulović, Jelena, Adžić, Miroslav, "Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression" in Behavioural Brain Research, 359 (2019):550-559,
https://doi.org/10.1016/j.bbr.2018.10.011 . .
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