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虎杖甙下调兔肺缺血再灌注损伤时TLR4的表达
引用本文:金晓凤,徐正衸,王万铁,许益笑.虎杖甙下调兔肺缺血再灌注损伤时TLR4的表达[J].中国病理生理杂志,2008,24(4):666-669.
作者姓名:金晓凤  徐正衸  王万铁  许益笑
作者单位:温州医学院病理生理学教研室,浙江 温州 325025
摘    要:目的: 研究家兔肺缺血再灌注损伤时Toll样受体4(TLR4)信号转导通路变化及虎杖甙(PD)对其影响。方法:复制在体肺缺血再灌注损伤模型。健康日本大耳白免30只, 随机分为对照(C)组、缺血再灌注(IR)组、PD组。鲎试剂试管法检测血浆内毒素(ET); 免疫组化法检测肺组织TLR4、核因子-κB p65(NF-κB p65)和热休克蛋白70(HSP70)的蛋白表达;原位杂交法检测肺组织细胞间黏附分子-1(ICAM-1)mRNA表达;电镜观察肺超微结构变化。结果:IR组、PD组与C组相比血浆ET无显著差异(均P>0.05)。IR组肺组织TLR4、NF-κB p65、HSP70蛋白及ICAM-1mRNA表达较C组显著升高(均P<0.01);PD组上述改变较IR组明显下降,但仍高于C组(均P<0.01); 电镜见PD组肺超微结构损伤明显轻于IR组。结论:肺缺血再灌注损伤过程中HSP70合成增加,作为内源性配体之一上调TLR4,可能通过激活NF-κB,进而诱导ICAM-1的转录和分泌。PD可以下调该信号转导途径,减轻肺缺血再灌注损伤。

关 键 词:虎杖甙    再灌注损伤  受体  Toll样  NF-κBp65  热休克蛋白质70  
文章编号:1000-4718(2008)04-0666-04
收稿时间:2006-9-13
修稿时间:2006年9月13日

Polydatin downregulates TLR4 expression in lung ischemia reperfusion injury in rabbits
JIN Xiao-feng,XU Zheng-jie,WANG Wan-tie,XU Yi-xiao.Polydatin downregulates TLR4 expression in lung ischemia reperfusion injury in rabbits[J].Chinese Journal of Pathophysiology,2008,24(4):666-669.
Authors:JIN Xiao-feng  XU Zheng-jie  WANG Wan-tie  XU Yi-xiao
Institution:Department of Pathophysioloy, Wenzhou Medical College, Wenzhou 325025, China. E-mail:xzjie@126.com
Abstract:AIM: To explore the influence of polydatin (PD) on Toll-like receptor 4 (TLR4) signal transduction pathway during lung ischemia reperfusion injury in rabbits. METHODS: Rabbit lung model of ischemia reperfusion (IR) injury was constituted in vivo. Thirty rabbits were divided into groups randomly: control (C), IR and PD group, respectively. The concentration of endotoxin (ET) in plasma was analyzed by end-point chromogenic assay. The protein expressions of TLR4, nuclear factor (NF)-κB p65 and heat shock protein 70 (HSP70) were measured by immunohistochemistry. The intracellular adhesion molecule-1 (ICAM-1) mRNA expression was detected by in situ hybridization histochemistry. The ultrastructural changes were observed by electron microscope. RESULTS: No significant difference of ET concentration in plasma between groups (all P>0.05) was observed. The protein expressions of TLR-4, NF-κB p65, HSP70 and ICAM-1mRNA in IR group were significantly increased as compared to C group and PD group, while those expressions in PD group were evidently higher than those in C group (all P<0.01). The lung pathological injuries in PD group were obviously alleviated as compared to IR group under electron microscope. CONCLUSION: It suggests that lung ischemia reperfusion releases endogenous ligands of TLR4 as HSP70, then activates NF-κB, promotes the release of mediators of inflammation such as ICAM-1. PD might have a protective effect on lung ischemia reperfusion injury by regulating TLR4 signal transduction pathway.
Keywords:Polydatin  Lung  Reperfusion injury  Receptors  Toll-like  NF-kappa B p65  Heat-shock proteins 70
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