Cuneyt Caglayan1, Fatih Mehmet Kandemir2, Ekrem Darendelioğlu3, Serkan Yıldırım4, Sefa Kucukler2, Muhammet Bahaeddin Dortbudak4. 1. Department of Biochemistry, Faculty of Veterinary Medicine, Bingol University, Bingol, 12000, Turkey. Electronic address: ccaglayan@bingol.edu.tr. 2. Department of Biochemistry, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey. 3. Department of Molecular Biology and Genetics, Faculty of Science and Literature, Bingol University, Bingol, Turkey. 4. Department of Pathology, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey.
Abstract
OBJECTIVE: Mercury is a global environmental pollutant and is responsible for several organ pathophysiology including oxidative stress-induced liver disorders. Therefore, the present study was conducted to evaluate the potential ameliorative effects of rutin on mercury chloride (HgCl2)-induced hepatotoxicity in adult male rats. METHODS: HgCl2 was intraperitoneally injected at a dose of 1.23 mg/kg body weight for 7 days alone or in combination with the orally rutin (50 and 100 mg/kg body weight). RESULTS: Rutin treatment significantly improved liver function tests [alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], and increased activities of antioxidant defense system [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] and glutathione (GSH) content. The histological alterations and epidermal growth factor receptor (EGFR) expression in the HgCl2-induced liver tissues were decreased by administration of rutin. Furthermore, rutin reversed the changes in levels of apoptosis and inflammation related proteins involving p53, Bcl-2 associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), cytochrome c, nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), B-cell lymphoma-3(Bcl-3) and interleukin-1β (IL-1β), and inhibited p38α mitogen-activated protein kinase (MAPK) and cysteine aspartate specific protease-3 (caspase-3) activations. CONCLUSION: The data of the present study suggest that rutin effectively suppress HgCl2-induced hepatotoxicity by ameliorating oxidative stress, inflammation and apoptosis.
OBJECTIVE:Mercury is a global environmental pollutant and is responsible for several organ pathophysiology including oxidative stress-induced liver disorders. Therefore, the present study was conducted to evaluate the potential ameliorative effects of rutin on mercury chloride (HgCl2)-induced hepatotoxicity in adult male rats. METHODS:HgCl2 was intraperitoneally injected at a dose of 1.23 mg/kg body weight for 7 days alone or in combination with the orally rutin (50 and 100 mg/kg body weight). RESULTS:Rutin treatment significantly improved liver function tests [alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT)], and increased activities of antioxidant defense system [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] and glutathione (GSH) content. The histological alterations and epidermal growth factor receptor (EGFR) expression in the HgCl2-induced liver tissues were decreased by administration of rutin. Furthermore, rutin reversed the changes in levels of apoptosis and inflammation related proteins involving p53, Bcl-2 associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), cytochrome c, nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), B-cell lymphoma-3(Bcl-3) and interleukin-1β (IL-1β), and inhibited p38α mitogen-activated protein kinase (MAPK) and cysteine aspartate specific protease-3 (caspase-3) activations. CONCLUSION: The data of the present study suggest that rutin effectively suppress HgCl2-induced hepatotoxicity by ameliorating oxidative stress, inflammation and apoptosis.
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