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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 observe the relationship between heat shock protein 70 inhibitor PFTμ and lipopolysaccharide-induced RAW264.7 cells and inflammatory response in mice with ischemia-reperfusion injury, and to explore its possible mechanism. Methods: RAW264.7 cells induced by lipopolysaccharide (LPS) were used to establish the cell inflammatory response model. The release of nitric oxide (NO) was measured by Griess reagent method. The expression of the target protein was determined by Western-Blot. The expression of inducible nitric oxide synthase (iNOS) mRNA was analyzed by enzyme linked immunosorbent assay (RT-PCR). The mouse model of myocardial ischemia-reperfusion (I / R) inflammation was established. Results: PFTμ, a heat shock protein 70 inhibitor, inhibited LPS-induced NO release in RAW264.7 cells, decreased iNOS protein and mRNA expression, and inhibited IκBα protein expression in early stage. At the same time, can reduce myocardial infarct size in ischemia-reperfusion mice. Conclusion: PFTμ can inhibit the inflammatory reaction and its mechanism may be through the inhibition of nitric oxide production.