Wang H, Peng R X, Wang R K, Kong R
Department of Pharmacology, Hubei Medical University, Wuhan 430071.
Yao Xue Xue Bao. 1997 Jul;32(7):511-4.
Effects of ethanol at different dosages on hepatic antioxidative and detoxicating functions and the antagonizing effect of sodium ferulate have been investigated in mice. The data showed that ethanol (11.4 g.kg-1, ig) could induce the increase of hepatic glutathione peroxidase (GSH-Px) activity and decreases of hepatic glutathione reductase (GSH-Re), superoxide dismutase (SOD) and glutathione S-transferase (GST) activities and reduce glutathione (GSH) content. At the same time, serum GST activity was increased. Pretreatment with sodium ferulate (100 mg.kg-1 ig, qd x 10 d) completely reversed these changes induced by ig ethanol in mice, indicating that sodium ferulate could protect mice from ethanol-induced acute hepatotoxicity. The hepato-protective mechanism of sodium ferulate may be related to intensification of the function of glutathione oxidative-reductive enzymes, enhancement of SOD activity and promotion of glutathione conjugation. The results also indicate that the serum GST level is a sensitive indicator in ethanol-induced hepatotoxicity.
研究了不同剂量乙醇对小鼠肝脏抗氧化和解毒功能的影响以及阿魏酸钠的拮抗作用。数据表明，乙醇（11.4 g·kg-1，灌胃）可诱导肝脏谷胱甘肽过氧化物酶（GSH-Px）活性升高，肝脏谷胱甘肽还原酶（GSH-Re）、超氧化物歧化酶（SOD）和谷胱甘肽S-转移酶（GST）活性及还原型谷胱甘肽（GSH）含量降低。同时，血清GST活性升高。阿魏酸钠预处理（100 mg·kg-1灌胃，每日1次，共10天）可完全逆转灌胃乙醇诱导的小鼠上述变化，表明阿魏酸钠可保护小鼠免受乙醇诱导的急性肝毒性。阿魏酸钠的肝保护机制可能与增强谷胱甘肽氧化还原酶功能、提高SOD活性及促进谷胱甘肽结合有关。结果还表明，血清GST水平是乙醇诱导肝毒性的敏感指标。
