文献类型：期刊文献

中文题名：细胞外热休克蛋白72作为Toll样受体内源性配体在大鼠缺血再灌注肝损伤中的表达及作用

英文题名：Expression and effect of extracellular heat-shock protein 72 as Toll-like receptor endogenous ligand on hepatic ischemia-reperfusion injury in rats

作者：朱冬芳[1];晏春根[2];黄丹文[3]

机构：[1]绍兴文理学院附属医院检验科;[2]绍兴文理学院附属医院消化内科;[3]绍兴文理学院附属医院肝病科

年份：2012

卷号：5

期号：3

起止页码：6

中文期刊名：中华危重症医学杂志：电子版

收录：CSTPCD

基金：浙江省自然科学基金项目(Y2100961);浙江省科技计划项目(2009C33129)

语种：中文

中文关键词：HSP72热休克蛋白质类;Toll样受体;再灌注损伤

外文关键词：HSP72 heat-shock proteins; Toll-like receptors; Reperfusion injury

中文摘要：目的探讨在大鼠缺血再灌注(I/R)肝损伤中,细胞外热休克蛋白72(HSP72)作为Toll样受体(TLR)内源性配体的表达及作用。方法将120只I/R组SD大鼠分为4组,每组30只,均予以I/R处理,其中A组于I/R处理前给予抗HSP72,B组给予重组HSP72,D组给予缺血预处理。同时以假手术组(P组,30只)及非手术组(N组,10只)为对照。之后于不同时间点采集标本,检测血浆丙氨酸转氨酶(ALT)、肿瘤坏死因子α(TNF-α)、HSP72及肝组织HSP72mRNA及其蛋白。结果 P组术后血浆TNF-α、HSP72水平较术前均显著升高(P均<0.01)。B组处理后相较I/R组其他分组,血浆ALT、TNF-α、HSP72均显著升高(P均<0.01)。P组及I/R各组的肝组织HSP72mRNA较术前均显著升高,且I/R各组升高较P组更为明显(P<0.01)。结论大鼠肝组织I/R后释放的HSP72可能启动了TLR信号通路,从而导致肝细胞的炎性损伤。

外文摘要：Objective To explore the expression and effect of extracellular heat-shock protein 72 （HSP72） regarded as endogenous ligand of Toll-like receptors on hepatic ischemia- reperfusion （I/R） injury in rats. Methods A total of 120 SD rats in the I/R group were randomly divided into 4 groups （30 in each and were all encountered I/R injury）. Before being I/R injury, group A and B were injected anti-HSP72 antibody and HSP72, respectively, and group D received ischemic precondition. The rats in the sham operation group （P group, 30 rats） and non-operation group （N group, 10 rats） were classified as controls. The levels of alanine aminotransferase （ALT）, tumor necrosis factor-alpha （TNF-o0, HSP72 in blood and the expressions of HSP72 mRNA and protein in liver tissue were detected at different time points with each group. Results After the treatment, the levels of TNF-α and HSP72 in the P group obviously increased （all P〈 0.01）, and the ALT, TNF-α and HSP72 in the B group were higher than other groups in the I/R group （all P〈0.01）. The HSP72 mRNA in the P and I/R groups also significantly increased after the treatment （all P〈 0.01）, and the I/R group were much higher （P〈 0.01）. Conclusion The HSP72 may activate the signal transduction pathways mediated by TLR and lead to inflammatory damage of hepatocyte after hepatic I/R injury.