目的:探讨间充质干细胞条件培养基(MSC-CM)对炎症介导的肺动脉血管平滑肌细胞(PASMC)增殖的调控机制.方法:取4～6代处于对数生长期人脐带MSC,建立体外细胞培养体系,分为对照组(PASMC)、T淋巴细胞刺激组(PASMC +T淋巴细胞)、MSC-CM干预组(PMSMC + T淋巴细胞+ MSC-CM);分别于培养第3天时,检测3组培养上清中肿瘤坏死因子(TNF)-α含量、PASMC的增殖、钙调神经磷酸酶(CaN)活性及活化的T淋巴细胞核因子2(NFATc2)活化情况.结果:与T淋巴细胞刺激组比较,MSC-CM干预组TNF-α的生成显著减少(P<0.0l);与对照组和T淋巴细胞刺激组比较,MSC-CM干预组的PASMC内CaN的磷酸酶活性降低、NFATc2的活化减少,PASMC的增殖降低(P<0.01).结论:MSC-CM可能通过CaN/NFAT信号通路抑制炎症介导的PASMC增殖.%Objective: To investigate the regulatory mechanism of Mesenchymal Stem Cell conditioned medium(MSC-CM) on proliferation of pulmonary artery smooth muscle cells(PASMC) mediated by inflammation. Methods: In vitro cell culture system was established by taking MSC from human umbilical cord at logarithmic growth stage and divided into control group(PASMC), T lymphocyte stimulation group(PASMC + T lymphocyte) and MSC-CM intervention group(PASMC + T lymphocyte + MSC-CM). On the third day of culture, the levels of tumor necrosis factor(TNF) -a in culture supernatant , proliferation of PASMC , CaN activity and activated NFATc2 were assessed. Results: The production of TNF-a in MSC-CM intervention group was significantly lower than that in T-lymphocyte stimulation group(P＜0.01). Compared with control group and T lymphocyte stimulation group, the activity of CaN phosphatase in PASMC of MSC-CM intervention group was decreased, activation of NFATc2 was reduced, and the proliferation of PASMC was reduced(P＜0.01). Conclusion: MSC-CM inhibits the proliferation of PASMC mediated by inflammation through the CaN/NFAT signaling pathway.
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