摘要
目的 观察了C反应蛋白（CRP）对培养的肺动脉平滑肌细胞（hPASMCs）炎性因子白介素-6（IL-6）的影响,探讨CRP对肺血管疾病的可能作用.方法 体外培养hPASMCs,以不同质量浓度的CRP（5～200μg/mL）刺激不同时间（0,3,6,9,12,18,24 h）.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.IL-6 mRNA和蛋白水平以Real-time PCR和ELISA方法进行检测.结果 CRP以浓度依赖的方式促进hPASMCs IL-6的合成.与对照组相比,CRP 200 μg/mL使IL-6的合成增加2.8倍.CRP显著诱导NF-κB在bPASMCs的激活.CRP对hPASMCs的促炎作用受到细胞表面FCγⅡa受体特异性抗体的抑制.结论 CRP促进体外培养的hPASMCs对IL-6的表达,这一作用是通过细胞表而FcγⅡa受体亚型和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.
Objective To examine the impact of C-reactive protein （CRP） on the expression of interleukin-6 （IL-6）, inflammatory cytokine, in cultured human pulmonary artery smooth muscle cells （hPASMCs） in order to find out the cause of pulmonary artery hypertension （PAH）. Method The hPASMCs were cultured and stimulated by different concerntrations of CRP （5 - 200 μg/ml） for different lengths of time. The activity of nuclear factor-κB （NF-κB） was evaluated by electrophoretic gel mobility shift assay （EMSA）. The expression of IL-6 mRNA and the level of IL-6 protein were measured by using real-time PCR and ELISA, respectively. Results CRP increased IL-6 production in hPASMCs in a dose-dependent manner. The increase in IL-6 at concerntration of 200 μg/mL in the CRP group was as high as 2.8times that in the control group. CRP also significantly induced the activation of NF-κB in hPASMCs. The effect of CRP on the inflammatory cytokine, IL-6, was inhibited by the specific FcγⅡa receptor antibody.Conclusions In vitro, CRP increases the production of IL-6 in hPASMCs mediated by FcγⅡa receptor and NF-κB translocation. These data offer important insights into the role of CRP in the pathogenesis of PAH.
出处
《中华急诊医学杂志》
CAS
CSCD
北大核心
2011年第4期395-399,共5页
Chinese Journal of Emergency Medicine
关键词
肺动脉平滑肌细胞
C反应蛋白
炎症
FcγⅡa受体
核因子ΚB
白介素-6
肺动脉高压
Pulmonary artery smooth muscle cells
C-reactive protein
Inflammation
FcγⅡa receptor
Nuclear factor κB
Interleukin -6
Pulmonary artery hypertension
