School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan;
Department of Nutrition, I-Shou University, Kaohsiung, Taiwan;
Hepatobiliary Surg Nutr. 2013 Jun;2(3):132-41. doi: 10.3978/j.issn.2304-3881.2013.06.08.
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.
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.
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.
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.
乙醇摄入可能诱导肝凋亡并导致肝损伤。本研究旨在探讨不同剂量β-胡萝卜素补充对慢性乙醇喂养大鼠抗氧化能力和肝凋亡的影响。
将大鼠分为 6 组:C(对照液体饮食)、CLB(对照液体饮食+β-胡萝卜素 0.52mg/kg 体重/天)、CHB(对照液体饮食+β-胡萝卜素 2.6mg/kg 体重/天)、E(乙醇液体饮食)、ELB(乙醇液体饮食+β-胡萝卜素 0.52mg/kg 体重/天)和 EHB(乙醇液体饮食+β-胡萝卜素 2.6mg/kg 体重/天)。12 周后处死大鼠,采集血液和肝脏样本进行分析。
E 组大鼠的脂质过氧化和肝细胞色素 P4502E1(CYP2E1)表达增加,Fas 配体、caspase-8、细胞色素 c、caspase-9 和 -3 的表达明显增加。然而,ELB 组大鼠的脂质过氧化和 CYP2E1、caspase-9 和 -3 的表达明显降低,Bcl-xL 的表达明显升高。EHB 组大鼠的肿瘤坏死因子(TNF)-α水平、脂质过氧化和细胞色素 c 的表达明显降低,Bcl-2 的表达明显升高。
这些结果表明,乙醇处理导致氧化应激和肝凋亡导致肝损伤,而β-胡萝卜素补充(0.52mg/kg 体重/天)可以通过降低乙醇诱导的氧化应激和抑制肝脏凋亡来预防乙醇引起的肝损伤。