Objectives: To investigate the protective effect of hesperidin and hesperetin against oxidative stress in 2,2'-azobis (2-aminopropane) dihydrochloride (AAPH)-induced liver toxicity in rats.
Methods: Hesperidin or hesperetin (200 mg/kg/day, respective...
Objectives: To investigate the protective effect of hesperidin and hesperetin against oxidative stress in 2,2'-azobis (2-aminopropane) dihydrochloride (AAPH)-induced liver toxicity in rats.
Methods: Hesperidin or hesperetin (200 mg/kg/day, respectively) was orally administered for 7 days once daily in rats. Subsequently, AAPH (50 mg/kg/day) was administered intraperitoneally. Lipid peroxidation, nitric oxide production, catalase activity, and protein expressions of nuclear factor-kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the liver tissues were measured.
Results: Administration of hesperidin and hesperetin significantly decreased serum aspartate transaminase and alanine transaminase levels in AAPH-induced oxidative stress liver tissues compared with control group. Lipid peroxidation and nitric oxide (NO) production were also significantly reduced by hesperidin and hesperetin in AAPH-induced oxidative stress liver tissues. In particular, lipid peroxidation levels of hesperetin-administered group significantly decreased to 5.02 nmole/mg protein in oxidative stress rats. Hesperidin and hesperetin significantly increased antioxidant activity, such as that of catalase. Furthermore, administration of hesperidin and hesperetin substantially down-regulated the expression of NF-κB and iNOS in liver tissues. Administration of hesperidin reduced NO levels and iNOS expression more than in the hesperetin-administered group.
Conclusions: Administration of hesperidin and hesperetin led to a reduction in AAPH-induced liver toxicity by regulating oxidative stress.