The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats

Hsiang-Chi Peng, Ya-Ling Chen, Shin-Yi Yang, Pei-Yin Ho, Sien-Sing Yang, Jui-Ting Hu, Suh-Ching Yang

Abstract

Background: Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.
Methods: Rats were divided into 6 groups: C (control liquid diet), CLB (control liquid diet with β-carotene supplementation at 0.52 mg/kg body weight (BW)/day], CHB (control liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day), E (ethanol liquid diet), ELB (ethanol liquid diet with β-carotene supplementation at 0.52 mg/kg BW/day), and EHB (ethanol liquid diet with β-carotene supplementation at 2.6 mg/kg BW/day). After 12 weeks, rats were sacrificed and blood and liver samples were collected for analysis.
Results: Lipid peroxidation and hepatic cytochrome P450 2E1 (CYP2E1) expression had increased, and hepatic Fas ligand, caspase-8, cytochrome c, caspase-9, and -3 expressions had significantly increased in the E group. However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group. The hepatic tumor necrosis factor (TNF)-α level, lipid peroxidation, and cytochrome c expression were significantly lower and Bcl-2 expression was significantly higher in the EHB group.
Conclusions: The results suggest that ethanol treatment causes oxidative stress and hepatic apoptosis leading to liver injury, and β-carotene supplementation (0.52 mg/kg BW/day) can prevent ethanol-induced liver damage by decreasing ethanol-induced oxidative stress and inhibiting apoptosis in the liver.