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目的:探讨阿托伐他汀(ATO)对人重组C反应蛋白(rhCRP)诱导的人动脉平滑肌细胞炎症反应的影响及其机制是否与下调妊娠相关性血浆蛋白-A(PAPP-A)、基质金属蛋白酶3(MMP3)mRNA表达相关。方法:应用不同浓度rhCRP(1、5、10、20 mg/L)处理人动脉平滑肌细胞不同时间(3、6、12、24 h),采用ELISA法检测炎症因子IL-6、IL-8水平,以确定炎症模型建立条件。不同时相点加入10~(-7)mol/L ATO后,ELISA法再次检测IL-6、IL-8水平;RT-PCR法测定PAPP-A、MMP3 mRNA表达水平。结果:不同浓度rhCRP处理人动脉平滑肌细胞不同时间后,人动脉平滑肌细胞培养基中的IL-6、IL-8呈浓度依赖性和时间依赖性增加(P<0.05)。采用10 mg/L rhCRP处理12 h作为人动脉平滑肌细胞炎症模型建立的条件。ATO 10-7 mol/L预处理、共处理均能有效抑制rhCRP所致的IL-6、IL-8升高(P<0.05),同时也能抑制rhCRP所致的PAPP-A、MMP3 mR NA表达升高(P<0.05);而ATO后处理组IL-6、IL-8水平及PAPP-A、MMP3 mRNA表达水平与rhCRP模型组比较,差异无统计学意义(P>0.05)。结论:AT0具有抑制出CRP诱导的人动脉平滑肌细胞炎症反应的作用,此作用可能与其下调PAPP-A、MMP3 mRNA表达有关。
AIM: To investigate the effect of atorvastatin (ATO) on the inflammatory response induced by rhCRP in human arterial smooth muscle cells and whether its mechanism may be associated with down-regulation of pregnancy-associated plasma protein-A (PAPP-A) Protease 3 (MMP3) mRNA expression. Methods: Human vascular smooth muscle cells were treated with different concentrations of rhCRP (1, 5, 10, 20 mg / L) for different time periods (3, 6, 12, 24 h). The levels of IL-6 and IL- To determine the conditions under which the inflammatory model was established. IL-6 and IL-8 levels were detected again by ELISA after adding 10 -7 mol / L ATO at different time points. The PAPP-A and MMP3 mRNA levels were determined by RT-PCR. Results: IL-6 and IL-8 in human arterial smooth muscle cells increased in a concentration-dependent manner and a time-dependent manner (P <0.05) after treated with different concentrations of rhCRP for different time. The condition of human smooth muscle cell inflammation was established by using 10 mg / L rhCRP for 12 h. ATO 10-7 mol / L pretreatment and co-treatment could both effectively inhibit the increase of rhCRP-induced IL-6 and IL-8 (P <0.05) as well as inhibit the PAPP-A and MMP3 mR NA induced by rhCRP (P <0.05). However, the levels of IL-6, IL-8 and PAPP-A, MMP3 mRNA in ATO group were not significantly different from those in rhCRP group (P> 0.05). CONCLUSION: AT0 can inhibit the inflammation induced by CRP in human aortic smooth muscle cells, which may be related to its downregulation of PAPP-A and MMP3 mRNA expression.