热休克蛋白70抑制剂PFTμ对炎症反应的影响

Research on the effects of HSP70 inhibtor on inflammatory response

目的:观察热休克蛋白70抑制剂PFTμ与脂多糖诱导RAW264.7细胞及缺血再灌注损伤小鼠炎症反应的关系,以探讨其影响和可能的作用机制。方法:采用脂多糖(LPS)诱导的RAW264.7细胞株建立细胞炎症反应模型,采用Griess试剂法测定一氧化氮(NO)释放量;采用Western-Blot法测定目的蛋白表达;采用反转录聚合酶链反应(RT-PCR)分析诱生型一氧化氮合酶(iNOS)mRNA表达改变;建立小鼠心脏缺血再灌注(I/R)炎症反应模型,测定小鼠心肌梗死面积。结果:热休克蛋白70抑制剂PFTμ可抑制LPS诱导的RAW264.7细胞NO的释放;下调iNOS蛋白和mRNA表达;早期可抑制IκBα蛋白的表达。同时,可减少缺血再灌注小鼠心肌梗死面积。结论:PFTμ有抑制炎症反应的作用,其作用机制可能是通过抑制一氧化氮的生成而发挥的。

OBJECTIVE To research the effects and mechanism of HSP70 inhibtor （PFTμ） on inflammation of LPS-induced RAW 264. 7 cells and myocardial ischemia-reperfusion （I/R） mice. METHODS RAW264. 7 macrophage line in mice was induced by LPS to set up the inflammatory model. The NO concentration was measured by Griess Kit. The expression of protein and mRNA were measured by Western-blot and RT-PCR. Cardiac ischemia-reperfusion （I/R） model was set up to study the inflammatory response in mice. The infarct size was monitored on myocardial isehemia-reperfusion （I/R） mice. RESULTS We found that PFTμ significantly blocked the production of NO and protein and mRNA expression of iNOS and inhibited IκBa protein early. We also investigated PFTμ, could reduce the infarct size on myocardial I/R mice. CONCLUSION These results suggest that PFTμ could be a useful adjunct in the treatment of inflammatory disease through inhibiting the production of NO.