姜黄素对乙醇诱导的大鼠原代肝细胞损伤的防护作用  

Protective Effect of Curcumin on Alcohol-Induced Oxidative Damage in Rat Primary Cultured Hepatocytes

作　　者：荣爽[1] 李珂[1] 宋方方[1] 刘爽[1] 姚平[1] 郝丽萍[1] 刘烈刚[1] 

机构地区：[1]华中科技大学同济医学院公共卫生学院营养与食品卫生系,湖北武汉430030

出　　处：《环境与健康杂志》2009年第6期487-489,共3页Journal of Environment and Health

基　　金：教育部新世纪优秀人才支持计划项目(NECT-04-0707)

摘　　要：目的研究姜黄素对乙醇诱导的大鼠原代肝细胞氧化损伤的防护作用。方法以二步胶原酶技术分离的SD大鼠原代肝细胞经不同剂量(0～200mmol/L)和不同时间(0～24h)暴露于乙醇,确定乙醇对肝细胞损伤的敏感的暴露时间与剂量。乙醇暴露前用姜黄素进行不同暴露剂量(0～50μmol/L)和暴露时间(0～5h)的预暴露。检测细胞培养上清液中天门冬氨酸氨基转移酶(AST)和乳酸脱氢酶(LDH)活力及肝细胞的氧化-抗氧化指标[谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)]来观察姜黄素对肝细胞免受乙醇氧化损伤的保护效应。结果与对照组相比,乙醇暴露组随着乙醇暴露浓度的增加和时间的增长,肝细胞培养液上清液中的LDH、AST活力和MDA水平升高,GSH含量和SOD活力下降。以100mmol/L暴露8h最为明显。与乙醇100mmol/L暴露8h组相比,姜黄素预暴露组(0～50μmol/L)随姜黄素剂量的增加,LDH、AST活力下降(P<0.05),姜黄素预暴露剂量为15和30μmol/L时接近对照组水平;MDA生成明显减少(P<0.05);但SOD、GSH水平明显升高(P<0.05),姜黄素预暴露剂量为15和30μmol/L时,SOD基本回复到对照组水平。15μmol/L姜黄素预暴露1和5h,各个指标与乙醇组相比,差异均有统计学意义,1h干预效果优于5h。结论姜黄素可能通过降低GSH消耗,提高抗氧化酶活力,抑制脂质过氧化来保护大鼠原代肝细胞的酒精性氧化损伤,保护作用与姜黄素剂量及暴露时间有关。Objective To study the protective effects of cureumin on oxidative damage induced by alcohol. Methods The rat primary hepatocytes were isolated and cultured by using two steps collagenase perfusion technique. The cells were treated with alcohol at different dosages （0-200 mmol/L） in different time（0-24 h） to definite the sensitive ethanol exposure dosage and time. On the basis of this, the bepatocytes were pre-treated with curcumin at different doses （0-50 μmo]/L） in different time （0-5 h） before ethanol exposure （100 mmol/L,8 h）.Then the activity of LDH, AST which released from hepatocyte and the cellular MDA, SOD,GSH were determined in order to observe the protection of curcumin and the time-dose-response effects. Results Compared with the normal hepatocytes, there was a great increase of AST and LDH release in the supernatants as well as MDA formation in hepatocytes, and a decrease of the level of GSH and SOD in ethanol group along with the increase of ethanol stimulate close and time, it was so obvious at 100 mmol/L or 8 h. Compared with the alcohol group, pre-treatment of cureumin could significantly prohibit the release of AST and LDH （P〈0.05）, the increase of MDA level （P〈0.05） and the decrease of SOD activities and GSH content （P〈0.05） of hepatocytes exposed to ethanol. The level of AST and LDH significantly increased in alcohol group and nearly reached to the same level as the normal group when the cureumin at the close of 15 μmol/L and 30 μmol/L respectively. And the SOD reached to the normal level at both 15 μmol/L and 30 μmol/L. The pre-treatment of cureumin （ 15 μmol/L）1 h and 5 h before alcohol exposure showed better protective effect than 0 h, and 1 h was the best. Conclusion Curcumin may prevent rat primary hepatoeytes from ethanol-induced oxidative damage probably by reducing GSH consumption, improving antioxidant enzyme activity and inhibiting lipid peroxidation reaction in close-dependent and time-dependent manner.

关 键 词：脂质过氧化 姜黄素 大鼠原代肝细胞 抗氧化酶 乙醇 氧化损伤 

分 类 号：R994.6[医药卫生—毒理学]