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目的:观察C反应蛋白(CRP)刺激人外周血单核细胞核因子-κB(NF-κB)活化及白细胞介素-6(IL-6)表达,予辛伐他汀干预,探讨CRP/NF-κB在动脉粥样硬化(AS)致病机制中的作用和辛伐他汀的抗AS效应。方法:密度梯度离心法分离人外周血单核细胞,免疫细胞化学观察CRP致单核细胞NF-κBp65活化的时间效应,ELISA法观察IL-6产生的时间-浓度效应,其峰值分别与辛伐他汀抑制剂组比较。结果:CRP刺激单核细胞NF-κB活化呈时间依赖性,高峰在2h,单核细胞表达IL-6呈时间与浓度依赖性,在24h达高峰。辛伐他汀(1×10-8mol/L～1×10-6mol/L)呈剂量依赖性抑制NF-κB活化与IL-6表达。结论:CRP激活正常人单核细胞NF-B信号途径,并诱导单核细胞产生IL-6,辛伐他汀抑制单核细胞NF-κB活性与IL-6表达,提示CRP/NF-κB信号途径在促进AS发病机制中起重要作用,辛伐他汀抑制NF-κB有可能减轻或抑制AS进展。
Objective: To observe the effects of C-reactive protein (CRP) on the activation of nuclear factor-κB (NF-κB) and interleukin-6 (IL-6) in peripheral blood mononuclear cells and the intervention of simvastatin to investigate the expression of CRP / NF- In the pathogenesis of atherosclerosis (AS) and the anti-AS effect of simvastatin. Methods: The mononuclear cells of human peripheral blood were isolated by density gradient centrifugation. The time effect of activation of NF-κB p65 induced by CRP was observed by immunocytochemistry. The time-concentration effect of IL-6 production was observed by ELISA. Statin inhibitor group comparison. Results: The activation of NF-κB induced by CRP in a time-dependent manner was peaked at 2 h. The expression of IL-6 in monocytes was time-dependent and concentration-dependent, reaching the peak at 24 h. Simvastatin (1 × 10-8mol / L ~ 1 × 10-6mol / L) inhibited NF-κB activation and IL-6 expression in a dose-dependent manner. CONCLUSIONS: CRP activates NF-κB signaling in normal human monocytes and induces monocytes to produce IL-6. Simvastatin inhibits NF-κB activity and IL-6 expression in monocytes, suggesting that CRP / NF-κB signaling pathway It plays an important role in promoting the pathogenesis of AS. Inhibition of NF-κB by simvastatin may reduce or inhibit the progression of AS.