CAJ | 학술논문

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.
목적 관찰료C반응단백(CRP)대배양적폐동맥평활기세포(hPASMCs)염성인자백개소-6(IL-6)적영향,탐토CRP대폐혈관질병적가능작용.방법 체외배양hPASMCs,이불동질량농도적CRP(5～200μg/mL)자격불동시간(0,3,6,9,12,18,24 h).핵인자κB(NF-κB)적활성이비변성응효전영천이솔(EMSA)방법진행분석.IL-6 mRNA화단백수평이Real-time PCR화ELISA방법진행검측.결과 CRP이농도의뢰적방식촉진hPASMCs IL-6적합성.여대조조상비,CRP 200 μg/mL사IL-6적합성증가2.8배.CRP현저유도NF-κB재bPASMCs적격활.CRP대hPASMCs적촉염작용수도세포표면FCγⅡa수체특이성항체적억제.결론 CRP촉진체외배양적hPASMCs대IL-6적표체,저일작용시통과세포표이FcγⅡa수체아형화NF-κB적핵내전위격활이개도적.제시CRP재폐동맥고압적발병중유중요작용.
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.