首页> 中文期刊> 《华中科技大学学报(医学版)》 >S100A9在小鼠脑缺血再灌注损伤中的表达及其意义

S100A9在小鼠脑缺血再灌注损伤中的表达及其意义

         

摘要

目的:探讨 S100A9在小鼠脑缺血再灌注损伤中的表达及其意义。方法将 Toll 样受体4(TLR4)基因突变型小鼠C3H/HeJ(n=21)和TLR4野生型 C3H/HeN 小鼠(n=21)分别随机分为野生型对照组(C3H/HeN 对照,n=8),突变型对照组(C3H/HeJ 对照,n=8),野生型模型组(C3H/HeN模型,n=13)以及突变型模型组(C3H/HeJ 模型,n=13),采用线栓法建立大脑中动脉栓塞模型,于再灌注12 h 后行神经功能缺损评分;TTC 染色测定脑梗死体积;苏木精-伊红染色评价脑组织损伤程度;免疫荧光成像和实时定量 PCR技术检测 S100A9蛋白及 mRNA 表达情况。结果C3 H/HeJ 模型组神经缺损评分低于C3 H/HeN模型组;脑梗死体积和神经细胞损伤程度也较 C3 H/HeN 模型组减轻;C3H/HeJ 和C3H/HeN模型组梗死侧脑组织中 S100A9 mRNA和蛋白较各自对照组表达均明显增高,且 C3H/HeJ 模型组脑组织中 S100A9表达量较 C3H/HeN 模型组明显减少。提示在脑缺血再灌注损伤时 S100A9蛋白表达与 TLR4关系密切。结论 S100A9有可能通过活化TLR4信号通路在脑缺血再灌注损伤过程中发挥重要作用。%Objective To investigate the expression of S100A9 in cerebral ischemia-reperfusion injury and it signifi-cance.Methods Toll-like receptor 4(TLR4)gene mutant mice C3H/HeJ(n=21)and TLR4 wild-type mice C3H/HeN(n=21) were randomly divided into four groups,which were C3H/HeN control group(n=8),C3H/HeJ control group(n=8),C3H/HeN model group(n=13)and C3H/HeJ model group(n=13).The model of focal ischemia was established by transient middle cerebral artery occlusion(MCAO).After reperfusion for 1 2 h,scoring for neurological deficit was performed;the brain infarcted size was evaluated by TTC staining;the brain damage was assessed by HE staining;S100A9 expression was detected by immu-nofluorescence staining and real-time PCR,respectively.Results The neurological deficit score was much lower in the C3 H/HeJ model group than in C3 H/HeN model group.The brain infarcted size and the brain damage were significantly attenuated in C3H/HeJ model group when compared with those in C3H/HeN model group.The mRNA and protein expression of S100A9 was significantly increased in C3 H/HeJ model group and C3 H/HeN model group as compared with that in their control groups.It was much lower in C3 H/HeJ model group than in C3 H/HeN model group.It was suggested that the expression of S100A9 protein was closely associated with TLR4 in cerebral ischemia-reperfusion injury.Conclusion S100A9 plays an impor-tant role in cerebral ischemia-reperfusion inj ury by activating the TLR4 signaling pathway.

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