Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats
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Trichloroethylene (TCE), a nephrotoxicant is known to cause severe damage to the kidney. In this study, the nephroprotective potential of hesperidin was evaluated against TCE-induced nephrotoxicity in wistar rats. Oral administration of TCE (1000 mg/kg b.wt) for 15 days enhanced renal lipid peroxidation and reduced antioxidant enzymes armoury viz., reduced renal glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, catalase and superoxide dismutase. It also enhanced the levels of blood urea nitrogen, creatinine and kidney injury molecule (KIM-1). Caspase-3 and bax expression were found to be elevated, while that of bcl-2 reduced suggesting that TCE induces apoptosis. However, pretreatment with hesperidin at a dose of 100 and 200 mg/kg b.wt for 15 days significantly decreased lipid peroxidation, increased the levels of antioxidant enzymes and reduced blood urea, creatinine and KIM-1 levels. Hesperidin also modulated the apoptotic pathways by altering the expressions of caspase-3, bax and bcl-2 to normal. Our results suggest that hesperidin can be used as a nephroprotective agent against TCE-induced nephrotoxicity.
KeywordsTrichloroethylene Nephrotoxicity Hesperidin Oxidative stress Apoptosis
Blood urea nitrogen
Kidney injury molecule
Reactive oxygen species
The author (SS), Jamia Hamdard University acknowledge the help given to the student (AS) for getting registered to PhD in Indira Gandhi National Open University, New Delhi, India.
Conflict of interest
The authors of the present research work do not have any conflict of interest.
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