title: Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats.
abstract: 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.
authors.affiliation: Discipline of Life Sciences, School of Sciences, Indira Gandhi National Open University, Maidan Garhi, New Delhi, 110068, India.
authors.forename: Aisha
authors.initials: A
authors.lastname: Siddiqi
authors.forename: Sana
authors.initials: S
authors.lastname: Nafees
authors.forename: Summya
authors.initials: S
authors.lastname: Rashid
authors.forename: Sarwat
authors.initials: S
authors.lastname: Sultana
authors.forename: Bano
authors.initials: B
authors.lastname: Saidullah
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006569:Hesperidin / Q000494:pharmacology* / Q000627:therapeutic use; D007668:Kidney / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar; D051437:Renal Insufficiency / Q000139:chemically induced / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014241:Trichloroethylene
chemical_list: D000975:Antioxidants; D051017:Apoptosis Regulatory Proteins; D014241:Trichloroethylene; D008315:Malondialdehyde; D006569:Hesperidin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione