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目的探讨机械牵张力刺激能否介导小鼠巨噬细胞活性氧族元素(ROS)的产生,并进一步探讨辛伐他汀对此作用的影响及其作用机制。方法体外常规培养小鼠巨噬细胞RAW264.7,施加机械力刺激,或用辛伐他汀预处理细胞60 min后再施加此刺激,用荧光探针H2DCFDA检测巨噬细胞ROS的表达水平,以细胞免疫荧光定量阳性率和SPSS统计软件对其表达水平进行分析。Western blot检测NADPH氧化酶1(NOX1)的表达。结果机械牵张力刺激介导的巨噬细胞ROS呈时间依赖性增多,以60 min最显著(P<0.05);辛伐他汀可抑制此刺激介导的巨噬细胞ROS表达增加,且抑制作用呈浓度依赖增强,以0.3μmol/L辛伐他汀的抑制作用最显著(P<0.05)。辛伐他汀可使机械牵张力介导的巨噬细胞NOX1表达显著减少。结论辛伐他汀可通过抑制NOX1的表达从而抑制由机械牵张力介导的小鼠巨噬细胞ROS的表达。
Objective To investigate whether mechanical stretch-stimulation can induce the production of reactive oxygen species (ROS) in mouse macrophages and further investigate the effect of simvastatin on it and its mechanism. Methods Macrophage RAW264.7 cells were cultured in vitro. The cells were stimulated with mechanical force or pretreated with simvastatin for 60 min. Then the cells were stimulated with fluorescent probe H2DCFDA to detect the level of ROS in macrophages. Immunofluorescence quantitative positive rate and SPSS statistical software to analyze its expression level. Western blot was used to detect the expression of NADPH oxidase 1 (NOX1). Results The ROS of macrophages stimulated by mechanical stretch stimulation increased in a time-dependent manner at 60 min (P <0.05). Simvastatin inhibited ROS-induced macrophage ROS expression and its inhibitory effect was inhibited The inhibitory effect of simvastatin 0.3μmol / L was the most significant (P <0.05). Simvastatin significantly reduced NOX1 expression in macrophages mediated by mechanical strain. Conclusion Simvastatin can inhibit the expression of ROS in mouse macrophages mediated by mechanical strain by inhibiting the expression of NOX1.