Toll样受体3在大鼠急性心肌梗死中作用机制.docVIP

Toll样受体3在大鼠急性心肌梗死中作用机制.doc

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Toll样受体3在大鼠急性心肌梗死中作用机制

Toll样受体3在大鼠急性心肌梗死中作用机制   [摘要] 目的 研究Toll样受体3(TLR3)在大鼠心肌梗死中的表达及作用机制。 方法 制备TLR3基因敲除大鼠及野生型大鼠,采用球囊结扎冠脉方法制作心肌梗死动物模型。随机分为野生型假手术组(n=15)、野生型心肌梗死组(n=15)、(TLR3-/-)假手术组(n=15)、(TLR3-/-)心肌梗死组(n=15)。检测心肌组织肌酸激酶同工酶(CK-MB)、肌钙蛋白cTnI含量;通过Western blot法检测Toll样受体3、NF-κB表达。 结果 与野生型心肌梗死组大鼠比较,(TLR3-/-)心肌梗死?M反映心肌损伤的CK-MB、cTnI减低;NF-κB表达降低;各组间差异均有统计学意义(P0.05)。 结论 TLR3基因缺失在急性心肌梗死中具有心脏保护作用,其保护机制与下调NF-κB表达,减轻心肌梗死炎症反应有关。   [关键词] TOLL样受体3;急性心肌梗死;核因子-κB;基因敲除   [中图分类号] R541;R392 [文献标识码] A [文章编号] 1673-9701(2018)01-0036-03   Mechanism of Toll-like receptor 3 in acute myocardial infarction in rats   WANG Yuanyuan1 CAO Jian2 DENG Li1   1.Department of Cardiology,the Third Hospital of Nanchang, Nanchang 330009,China; 2.Department of Anesthesiology,the Second Affiliated Hospital of Nanchang University,Nanchang, 330006,China   [Abstract] Objective To study the expression of Toll-like receptor 3(TLR3) in myocardial infarction of rats and its mechanism. Methods TLR3 gene knockout rats and wild-type rats were prepared. Animal models of myocardial infarction were created by balloon ligation of coronary arteries. The rats were randomly divided into wild-type sham surgery group (n=15), wild-type myocardial infarction group(n=15),(TLR3-/-)sham surgery group(n=15), and(TLR3-/-)myocardial infarction group(n=15). The creatine kinase(CK-MB)and troponin cTnI contents in myocardial tissues were measured. Toll-like receptor 3 and NF-κB expressions were detected by Western blot method. Results Compared with the rats in the wild-type myocardial infarction group, the levels of CK-MB and cTnI which reflected myocardial injury in the(TLR3-/-) myocardial infarction group were decreased; NF-κB expression was decreased; the differences between groups were statistically significant(P0.05). Conclusion TLR3 gene deletion has cardioprotective effects in acute myocardial infarction. Its protective mechanism is related to the down-regulation of NF-κB expression and alleviation of inflammatory response induced by myocardial infa

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