Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
The protective effect of astaxanthin against cisplatin-induced nephrotoxicity in rats.
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Akca Gorkem, Eren Huseyin, Tumkaya Levent, Mercantepe Tolga, Horsanali Mustafa Ozan, Deveci Ezgi, Dil Eyup, Yilmaz Adnan
Аннотация
PURPOSE: The aim of this experimental study was to investigate the antioxidant effects of astaxanthin against cisplatin-induced nephrotoxicity in rats.
METHODS: Forty-eight male Sprague-Dawley rats weighing 264.83 ± 7.39 g were randomly divided into six groups of eight animals each. These were constituted as control, olive oil control, astaxanthin control, cisplatin control, 16 mg/kg cisplatin & 25 mg/kg astaxanthin and 16 mg/kg cisplatin & 75 mg/kg astaxanthin groups. Biochemical evaluation was performed by measuring blood urea nitrogen, serum creatinine, total oxidant status and total antioxidant status. Renal corpuscle, proximal and distal tubules areas (μm2) were calculated for histopathological evaluation, and Caspase-3 staining was performed for immunohistochemical evaluation.
RESULTS: Cisplatin reduced total antioxidant status levels and increased blood urea nitrogen, serum creatinine, total oxidant status, and Caspase-3 levels. It also caused dilatation, vacuolization, and loss of tubular epithelial cells in the proximal and distal tubules, and glomerular degeneration and edema were determined in kidney tissue (p < 0.05). Administration of 25 mg and 75 mg astaxanthin increased total antioxidant status levels, reduced blood urea nitrogen, serum creatinine, total oxidant status, and Caspase-3, and ameliorated degenerative distal and proximal tubules, glomerular degeneration and edema in kidney tissue (p < 0.05).
CONCLUSIONS: The nephrotoxic effect of cisplatin was diminished by the antioxidant effect of astaxanthin.
METHODS: Forty-eight male Sprague-Dawley rats weighing 264.83 ± 7.39 g were randomly divided into six groups of eight animals each. These were constituted as control, olive oil control, astaxanthin control, cisplatin control, 16 mg/kg cisplatin & 25 mg/kg astaxanthin and 16 mg/kg cisplatin & 75 mg/kg astaxanthin groups. Biochemical evaluation was performed by measuring blood urea nitrogen, serum creatinine, total oxidant status and total antioxidant status. Renal corpuscle, proximal and distal tubules areas (μm2) were calculated for histopathological evaluation, and Caspase-3 staining was performed for immunohistochemical evaluation.
RESULTS: Cisplatin reduced total antioxidant status levels and increased blood urea nitrogen, serum creatinine, total oxidant status, and Caspase-3 levels. It also caused dilatation, vacuolization, and loss of tubular epithelial cells in the proximal and distal tubules, and glomerular degeneration and edema were determined in kidney tissue (p < 0.05). Administration of 25 mg and 75 mg astaxanthin increased total antioxidant status levels, reduced blood urea nitrogen, serum creatinine, total oxidant status, and Caspase-3, and ameliorated degenerative distal and proximal tubules, glomerular degeneration and edema in kidney tissue (p < 0.05).
CONCLUSIONS: The nephrotoxic effect of cisplatin was diminished by the antioxidant effect of astaxanthin.