Zarife N Özdemir-Kumral1, Burak E Erkek2, Buse Karakuş2, Meslina Almacı2, Reza Fathi1, Meral Yüksel3, Alev Cumbul4, İnci Alican5. 1. Department of Physiology, Marmara University School of Medicine, Maltepe, İstanbul, Turkey. 2. Department of Physiology, Marmara University School of Medicine, Year-3 Student, Maltepe, İstanbul, Turkey. 3. Department of Medical Laboratory-Biochemistry, Marmara University, Vocational School of Health Services, Kartal, İstanbul, Turkey. 4. Department of Histology and Embryology, Yeditepe University, School of Medicine, Ataşehir, İstanbul, Turkey. 5. Department of Physiology, Marmara University School of Medicine, Maltepe, İstanbul, Turkey. Electronic address: incialican@yahoo.com.
Abstract
BACKGROUND: 1,25 Dihydroxyvitamin D3 (1,25(OH)2D3) modulates inflammation and immune responses. Deficiency of 1,25(OH)2D3 was found to be associated with the risk of cancer, cardiovascular disease, osteoarthritis, infections, and autoimmune diseases. This study evaluated the effect of 1,25 dihydroxyvitamin D3 1,25(OH)2D3 on thioacetamide (TAA)-induced acute liver injury in rats. MATERIALS AND METHODS: Rats were treated with either saline or 1,25(OH)2D3 (0.30 μg/kg; orogastrically) for 15 d. Starting from day 13, TAA (200 mg/kg; intraperitoneally) was given for 3 d. On day 15, all rats were euthanized. Liver and blood samples were collected. RESULTS: TAA caused severe damage, increased lipid peroxidation with reductions in endogenous antioxidants, increased apoptosis, increased production of reactive oxygen species, and elevated inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-κB) expression in liver. Extent of damage was decreased by 1,25(OH)2D3 (P < 0.01). 1,25(OH)2D3 attenuated the increase in malondialdehyde (P < 0.01), increase in myeloperoxidase (P < 0.01), increase in chemiluminescence levels (P < 0.05) and apoptotic activity (P < 0.001). Elevated liver iNOS and NF-κB expression in TAA group was also reduced by 1,25(OH)2D3 (P < 0.001, for iNOS; P < 0.001, for NF-κB). TAA group revealed high serum aspartate transaminase and alanine transaminase (ALT) activities (P < 0.01, for aspartate transaminase; P = 0.08, for ALT) and reduced albumin levels (P < 0.01) compared with control. 1,25(OH)2D3 had no statistically significant effect on these parameters. CONCLUSIONS: 1,25(OH)2D3 provides protection against hepatic injury in a rat model of TAA-induced hepatotoxicity via suppression of inflammatory reaction, oxidative stress, and apoptosis.
BACKGROUND:1,25 Dihydroxyvitamin D3 (1,25(OH)2D3) modulates inflammation and immune responses. Deficiency of 1,25(OH)2D3 was found to be associated with the risk of cancer, cardiovascular disease, osteoarthritis, infections, and autoimmune diseases. This study evaluated the effect of 1,25 dihydroxyvitamin D3 1,25(OH)2D3 on thioacetamide (TAA)-induced acute liver injury in rats. MATERIALS AND METHODS:Rats were treated with either saline or 1,25(OH)2D3 (0.30 μg/kg; orogastrically) for 15 d. Starting from day 13, TAA (200 mg/kg; intraperitoneally) was given for 3 d. On day 15, all rats were euthanized. Liver and blood samples were collected. RESULTS: TAA caused severe damage, increased lipid peroxidation with reductions in endogenous antioxidants, increased apoptosis, increased production of reactive oxygen species, and elevated inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-κB) expression in liver. Extent of damage was decreased by 1,25(OH)2D3 (P < 0.01). 1,25(OH)2D3 attenuated the increase in malondialdehyde (P < 0.01), increase in myeloperoxidase (P < 0.01), increase in chemiluminescence levels (P < 0.05) and apoptotic activity (P < 0.001). Elevated liver iNOS and NF-κB expression in TAA group was also reduced by 1,25(OH)2D3 (P < 0.001, for iNOS; P < 0.001, for NF-κB). TAA group revealed high serum aspartate transaminase and alanine transaminase (ALT) activities (P < 0.01, for aspartate transaminase; P = 0.08, for ALT) and reduced albumin levels (P < 0.01) compared with control. 1,25(OH)2D3 had no statistically significant effect on these parameters. CONCLUSIONS:1,25(OH)2D3 provides protection against hepatic injury in a rat model of TAA-induced hepatotoxicity via suppression of inflammatory reaction, oxidative stress, and apoptosis.
Authors: Dalia Mahmoud Abdelmonem Elsherbini; Fatma M Ghoneim; Eman Mohammed El-Mancy; Hasnaa Ali Ebrahim; Mohamed El-Sherbiny; Mohamed El-Shafey; Rasha Hamed Al-Serwi; Nehal M Elsherbiny Journal: Front Cell Neurosci Date: 2022-08-17 Impact factor: 6.147
Authors: Elena B Menshchikova; Peter M Kozhin; Anton V Chechushkov; Marina V Khrapova; Nikolay K Zenkov Journal: Oxid Med Cell Longev Date: 2021-05-14 Impact factor: 6.543