TY  - JOUR
AU  - Vučević, Danijela B.
AU  - Borozan, Sunčica
AU  - Radenković, Ana S.
AU  - Radosavljević, Milica I.
AU  - Mladenović, Dušan R.
AU  - Jorgačević, Bojan Z.
AU  - Samardžić, Janko M.
AU  - Vesković, Milena N.
AU  - Vukičević, Dušan V.
AU  - Radosavljević, Tatjana S.
PY  - 2020
UR  - https://vet-erinar.vet.bg.ac.rs/handle/123456789/1861
AB  - Galectin-3 (Gal-3) has increasingly been recognized as a modulator of inflammation, oxidative/nitrosative stress, fibrogenesis, and tissue remodeling. The objective of the current pilot study was to investigate the influence of Gal-3 on cardiac and renal antioxidant capacity using biochemical and histopathological examinations. Two groups (n=7 each) of male mice were tested: 1. control (CON) group (wild type of C57BL/6 mice) and 2. GAL-3-/- group (galectin-3-/- knockout mice). After overnight fasting, mice were sacrificed by exsanguination in ketamine (100mg/kg intraperitoneally). Then, cardiac and renal tissue samples were taken to determine the parameters of oxidative/nitrosative stress and antioxidant capacity. The levels of malondialdehyde and nitrites+nitrates was not significantly different in the GAL-3-/- group vs. the CON group. The total superoxide dismutase activity in the renal tissue of the GAL-3-/- mice was significantly lower compared to the CON group. Cardiac and renal catalase and glutathione S-transferase activity was significantly reduced in the GAL-3-/- group vs. the CON group, respectively. A significant decrease in glutathione level was also registered in hearts of the GAL-3-/- group vs. the CON group. Our findings indicate that Gal-3 deficiency does not lead to lipid peroxidation and nitrosative stress in cardiac and renal tissue in mice. However, the lack of this beta-galactoside-binding lectin does reduce antioxidant capacity in both of the investigated tissues.
PB  - Institute of Systematics and Evolution of Animals
T2  - Folia Biologica (Poland)
T1  - Galectin-3 deficiency reduces cardiac and renal antioxidant capacity in mice
VL  - 68
IS  - 2
SP  - 73
EP  - 80
DO  - 10.3409/fb_68-2.09
ER  - 

@article{
author = "Vučević, Danijela B. and Borozan, Sunčica and Radenković, Ana S. and Radosavljević, Milica I. and Mladenović, Dušan R. and Jorgačević, Bojan Z. and Samardžić, Janko M. and Vesković, Milena N. and Vukičević, Dušan V. and Radosavljević, Tatjana S.",
year = "2020",
abstract = "Galectin-3 (Gal-3) has increasingly been recognized as a modulator of inflammation, oxidative/nitrosative stress, fibrogenesis, and tissue remodeling. The objective of the current pilot study was to investigate the influence of Gal-3 on cardiac and renal antioxidant capacity using biochemical and histopathological examinations. Two groups (n=7 each) of male mice were tested: 1. control (CON) group (wild type of C57BL/6 mice) and 2. GAL-3-/- group (galectin-3-/- knockout mice). After overnight fasting, mice were sacrificed by exsanguination in ketamine (100mg/kg intraperitoneally). Then, cardiac and renal tissue samples were taken to determine the parameters of oxidative/nitrosative stress and antioxidant capacity. The levels of malondialdehyde and nitrites+nitrates was not significantly different in the GAL-3-/- group vs. the CON group. The total superoxide dismutase activity in the renal tissue of the GAL-3-/- mice was significantly lower compared to the CON group. Cardiac and renal catalase and glutathione S-transferase activity was significantly reduced in the GAL-3-/- group vs. the CON group, respectively. A significant decrease in glutathione level was also registered in hearts of the GAL-3-/- group vs. the CON group. Our findings indicate that Gal-3 deficiency does not lead to lipid peroxidation and nitrosative stress in cardiac and renal tissue in mice. However, the lack of this beta-galactoside-binding lectin does reduce antioxidant capacity in both of the investigated tissues.",
publisher = "Institute of Systematics and Evolution of Animals",
journal = "Folia Biologica (Poland)",
title = "Galectin-3 deficiency reduces cardiac and renal antioxidant capacity in mice",
volume = "68",
number = "2",
pages = "73-80",
doi = "10.3409/fb_68-2.09"
}

Vučević, D. B., Borozan, S., Radenković, A. S., Radosavljević, M. I., Mladenović, D. R., Jorgačević, B. Z., Samardžić, J. M., Vesković, M. N., Vukičević, D. V.,& Radosavljević, T. S.. (2020). Galectin-3 deficiency reduces cardiac and renal antioxidant capacity in mice. in Folia Biologica (Poland)
Institute of Systematics and Evolution of Animals., 68(2), 73-80.
https://doi.org/10.3409/fb_68-2.09

Vučević DB, Borozan S, Radenković AS, Radosavljević MI, Mladenović DR, Jorgačević BZ, Samardžić JM, Vesković MN, Vukičević DV, Radosavljević TS. Galectin-3 deficiency reduces cardiac and renal antioxidant capacity in mice. in Folia Biologica (Poland). 2020;68(2):73-80.
doi:10.3409/fb_68-2.09 .

Vučević, Danijela B., Borozan, Sunčica, Radenković, Ana S., Radosavljević, Milica I., Mladenović, Dušan R., Jorgačević, Bojan Z., Samardžić, Janko M., Vesković, Milena N., Vukičević, Dušan V., Radosavljević, Tatjana S., "Galectin-3 deficiency reduces cardiac and renal antioxidant capacity in mice" in Folia Biologica (Poland), 68, no. 2 (2020):73-80,
https://doi.org/10.3409/fb_68-2.09 . .

TY  - JOUR
AU  - Vesković, Milena
AU  - Mladenović, Dušan
AU  - Milenković, Marina
AU  - Tosić, Jelena
AU  - Borozan, Sunčica
AU  - Gopcević, Kristina
AU  - Labudović-Borović, Milica
AU  - Dragutinović, Vesna
AU  - Vučević, Dragana
AU  - Jorgacević, Bojan
AU  - Isaković, Aleksandra
AU  - Trajković, Vladimir
AU  - Radosavljević, Tatjana
PY  - 2019
UR  - https://vet-erinar.vet.bg.ac.rs/handle/123456789/1727
AB  - We examined the effects of betaine, an endogenous and dietary methyl donor essential for the methionine-homocysteine cycle, on oxidative stress, inflammation, apoptosis, and autophagy in methionine-choline deficient diet (MCD)-induced non-alcoholic fatty liver disease (NAFLD). Male C57BL/6 mice received standard chow (control), standard chow and betaine (1.5% w/v in drinking water), MCD, or MCD and betaine. After six weeks, serum and liver samples were collected for analysis. Betaine reduced MCD-induced increase in liver transaminases and inflammatory infiltration, as well as hepatosteatosis and serum levels of low-density lipoprotein, while it increased that of high-density lipoprotein. MCD-induced hepatic production of reactive oxygen and nitrogen species was significantly reduced by betaine, which also improved liver antioxidative defense by increasing glutathione content and superoxide-dismutase, catalase, glutathione peroxidase, and paraoxonase activity. Betaine reduced the liver expression of proinflammatory cytokines tumor necrosis factor and interleukin-6, as well as that of proapoptotic mediator Box, while increasing the levels of anti-inflammatory cytokine interleukin-10 and antiapoptotic Bcl-2 in MCD-fed mice. In addition, betaine increased the expression of autophagy activators beclin 1, autophagy-related (Atg)4 and Atg5, as well as the presence of autophagic vesicles and degradation of autophagic target sequestosome 1/p62 in the liver of NAFLD mice. The observed effects of betaine coincided with the increase in the hepatic phosphorylation of mammalian target of rapamycin (mTOR) and its activator Akt. In conclusion, the beneficial effect of betaine in MCD-induced NAFLD is associated with the reduction of liver oxidative stress, inflammation, and apoptosis, and the increase in cytoprotective Akt/mTOR signaling and autophagy.
PB  - Elsevier Science Bv, Amsterdam
T2  - European Journal of Pharmacology
T1  - Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease
VL  - 848
SP  - 39
EP  - 48
DO  - 10.1016/j.ejphar.2019.01.043
ER  - 

@article{
author = "Vesković, Milena and Mladenović, Dušan and Milenković, Marina and Tosić, Jelena and Borozan, Sunčica and Gopcević, Kristina and Labudović-Borović, Milica and Dragutinović, Vesna and Vučević, Dragana and Jorgacević, Bojan and Isaković, Aleksandra and Trajković, Vladimir and Radosavljević, Tatjana",
year = "2019",
abstract = "We examined the effects of betaine, an endogenous and dietary methyl donor essential for the methionine-homocysteine cycle, on oxidative stress, inflammation, apoptosis, and autophagy in methionine-choline deficient diet (MCD)-induced non-alcoholic fatty liver disease (NAFLD). Male C57BL/6 mice received standard chow (control), standard chow and betaine (1.5% w/v in drinking water), MCD, or MCD and betaine. After six weeks, serum and liver samples were collected for analysis. Betaine reduced MCD-induced increase in liver transaminases and inflammatory infiltration, as well as hepatosteatosis and serum levels of low-density lipoprotein, while it increased that of high-density lipoprotein. MCD-induced hepatic production of reactive oxygen and nitrogen species was significantly reduced by betaine, which also improved liver antioxidative defense by increasing glutathione content and superoxide-dismutase, catalase, glutathione peroxidase, and paraoxonase activity. Betaine reduced the liver expression of proinflammatory cytokines tumor necrosis factor and interleukin-6, as well as that of proapoptotic mediator Box, while increasing the levels of anti-inflammatory cytokine interleukin-10 and antiapoptotic Bcl-2 in MCD-fed mice. In addition, betaine increased the expression of autophagy activators beclin 1, autophagy-related (Atg)4 and Atg5, as well as the presence of autophagic vesicles and degradation of autophagic target sequestosome 1/p62 in the liver of NAFLD mice. The observed effects of betaine coincided with the increase in the hepatic phosphorylation of mammalian target of rapamycin (mTOR) and its activator Akt. In conclusion, the beneficial effect of betaine in MCD-induced NAFLD is associated with the reduction of liver oxidative stress, inflammation, and apoptosis, and the increase in cytoprotective Akt/mTOR signaling and autophagy.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "European Journal of Pharmacology",
title = "Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease",
volume = "848",
pages = "39-48",
doi = "10.1016/j.ejphar.2019.01.043"
}

Vesković, M., Mladenović, D., Milenković, M., Tosić, J., Borozan, S., Gopcević, K., Labudović-Borović, M., Dragutinović, V., Vučević, D., Jorgacević, B., Isaković, A., Trajković, V.,& Radosavljević, T.. (2019). Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease. in European Journal of Pharmacology
Elsevier Science Bv, Amsterdam., 848, 39-48.
https://doi.org/10.1016/j.ejphar.2019.01.043

Vesković M, Mladenović D, Milenković M, Tosić J, Borozan S, Gopcević K, Labudović-Borović M, Dragutinović V, Vučević D, Jorgacević B, Isaković A, Trajković V, Radosavljević T. Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease. in European Journal of Pharmacology. 2019;848:39-48.
doi:10.1016/j.ejphar.2019.01.043 .

Vesković, Milena, Mladenović, Dušan, Milenković, Marina, Tosić, Jelena, Borozan, Sunčica, Gopcević, Kristina, Labudović-Borović, Milica, Dragutinović, Vesna, Vučević, Dragana, Jorgacević, Bojan, Isaković, Aleksandra, Trajković, Vladimir, Radosavljević, Tatjana, "Betaine modulates oxidative stress, inflammation, apoptosis, autophagy, and Akt/mTOR signaling in methionine-choline deficiency-induced fatty liver disease" in European Journal of Pharmacology, 848 (2019):39-48,
https://doi.org/10.1016/j.ejphar.2019.01.043 . .