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目的近年的研究显示,炎症参与肺动脉高压的发生和发展。作为炎症的重要指标,C反应蛋白(CRP)是肺动脉高压的独立预测因子。本文通过观察CRP和阿托伐他汀对培养的肺动脉平滑肌细胞(hPASMCs)增殖的影响,探讨CRP和阿托伐他汀对肺血管疾病的可能作用。方法体外培养hPASMCs,以不同浓度的CRP(5-200μg/ml)刺激24h,或先加阿托伐他汀(0.1-10μmol/l)处理2h。核因子κB(NF-κB)的活性以非变性凝胶电泳迁移率(EMSA)方法进行分析。细胞增殖水平以5-溴脱氧尿嘧啶核苷(BrDU)掺入法和ELISA方法进行检测。结果 CRP刺激hPASMCs的增殖程度呈浓度依赖性,随着CRP浓度的增加,细胞增殖倍数逐渐上升,在CRP200μg/ml组,其增殖倍数为对照组的1.84±0.12(P<0.001)。CRP显著诱导NF-κB在hPASMCs中的激活。阿托伐他汀则通过抑制NF-κB的激活而减轻hPASMCs的增殖。结论 CRP促进肺动脉平滑肌细胞的增殖,具有浓度依赖性,这一作用是通过对NF-κB的核内转位激活而介导的。提示CRP在肺动脉高压的发病中有重要作用,阿托伐他汀可能对肺血管疾病有保护作用。
Purpose Recent studies have shown that inflammation is involved in the occurrence and development of pulmonary hypertension. As an important indicator of inflammation, C-reactive protein (CRP) is an independent predictor of pulmonary hypertension. In this paper, CRP and atorvastatin on proliferation of cultured pulmonary artery smooth muscle cells (hPASMCs) were observed to explore the possible role of CRP and atorvastatin on pulmonary vascular disease. Methods hPASMCs were cultured in vitro, stimulated with different concentrations of CRP (5-200μg / ml) for 24h, or treated with atorvastatin (0.1-10μmol / l) for 2h. The activity of nuclear factor kappa B (NF-κB) was analyzed by the non-denaturing gel electrophoresis mobility shift assay (EMSA). The level of cell proliferation was detected by 5-bromodeoxyuridine (BrDU) incorporation and ELISA. Results The proliferation of CRP-stimulated hPASMCs was concentration-dependent. With the increase of CRP concentration, the multiplication rate of CRP increased gradually. In CRP200μg / ml group, the multiplication rate of CRP was 1.84 ± 0.12 (P <0.001) in control group. CRP significantly induced the activation of NF-κB in hPASMCs. Atorvastatin decreased the proliferation of hPASMCs by inhibiting the activation of NF-κB. Conclusion CRP can promote the proliferation of pulmonary artery smooth muscle cells in a concentration-dependent manner, which is mediated through the activation of nuclear translocation of NF-κB. Tip CRP plays an important role in the pathogenesis of pulmonary hypertension, atorvastatin may have a protective effect on pulmonary vascular disease.