文献类型：期刊文献

中文题名：N-乙酰半胱氨酸对肝缺血再灌注损伤大鼠Toll样受体4表达的影响

英文题名：Effect of N-acetylcysteine on expression of Toll-like receptor 4 of rats with hepatic ischemia-reperfusion injury

作者：晏春根[1];谢青[2]

机构：[1]绍兴文理学院医学院附属医院;[2]上海交通大学医学院附属瑞金医院

年份：2006

卷号：25

期号：7

起止页码：481

中文期刊名：中国新药与临床杂志

外文期刊名：Chinese Journal of New Drugs and Clinical Remedies

收录：CSTPCD、、北大核心2004、CSCD2011_2012、北大核心、CSCD

语种：中文

中文关键词：再灌注损伤;大鼠;Toll样受体4;N-乙酰半胱氨酸

外文关键词：reperfusion injury; rats; Toll-like receptor 4; N-acetylcysteine

中文摘要：目的：探讨N-乙酰半胱氨酸(N-acetylcysteine,NAC)对肝缺血再灌注(ischemic reperfusion,I/R)损伤大鼠Toll样受体4(Toll-like receptor 4,TLR4)表达的影响。方法：Wistar大鼠随机分为3组：假手术组(P)、I/R组、I/R+NAC组。P组只开腹不阻断肝血流,另2组阻断大部肝血流后再灌注,其中I/R+NAC组再灌注前5 min尾静脉给予300 mg/kg NAC。各组分别检测不同时间点的血丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、脂多糖(LPS)与肝组织TLR4 mRNA及其蛋白。结果：在各时间点,P组血ALT,AST,LPS和肝绍织TLR4表达无显著差异；另2组较P组均有显著升高,但I/R+NAC组各指标升高低于I/R组。肝组织TLR4 mRNA表达在I/R组从3 h起显著增强并维持高表达,而I/R+NAC组各时相无显著变化；但两者TLR4蛋白表达变化类似,都在6,24 h表达显著增强。结论：LPS及其TLR4参与了I/R肝损伤的病理过程；NAC减弱肠源性LPS及其启动的TLR4炎症信号通路而保护缺血再灌注肝损伤。

外文摘要：AIM： To explore the role of N-acetylcysteine （NAC） on the expression of Toll-like receptor 4 of rats with hepatic ischemia-reperfusion （I/R） injury. METHODS：Wistar rats were divided into three groups： the pseud-operated control （P） group, I/R group, and I/R＋NAC group treated with NAC intra-tail vein administration with dose of 300 mg.kg^-1 at 5 min before reperfusion. The concentrations of serum alanine aminotransferase（ALT）, aspartate aminotransferase （AST） and plasma lipopolysaccharide （LPS） at various period-point were measured. The expression of TLR4 protein and mRNA of liver tissue were detected with immunohistochemistry and reverse transcription-polymerase chain reaction （RT-PCR）. RESULTS： The levels of ALT, AST, and LPS were markedly increased during hepatic ischemia and reperfusion, but they were lower in I/R＋NAC group and nearly no alteration in P group. The expression of TLR4 mRNA in I/R group was significantly arised at 3 h after I/R hepatic injury and maintained high level but with no change in I/R＋NAC group. The expressions of TLR4 protein were similar between I/R and I/R＋NAC group at various time-point. CONCLUSION ： LPS and TLR4 play a prominent role in the pathophysiological processes of I/R hepatic injury and NAC can reduce endotoxemia derived from gut, inhibit the inflammatory pathway induced by LPS and TLR4, and protect the I/R hepatic injury.