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目的 研究前炎症细胞因子对人胸膜间皮细胞 (HPMC)释放纤溶酶原激活物抑制剂(PAI 1)的诱导效应。方法 渗出性胸膜腔积液的 6份原代HPMC置于DMEM/F12培养液中体外孵育 ,观察前炎症细胞因子白细胞介素 1β(IL 1β)和肿瘤坏死因子 α(TNF α)对HPMC纤溶活动的影响。对分离的HPMC纯度进行光镜下细胞学形态、电镜下超微结构和免疫组化染色的鉴定 ,加入IL 1β或TNF α诱导培养第三代HPMC 2 4小时后对HPMC培养液中PAI 1活性采用底物显色法进行测定。结果 与对照组相比 ,下列三种浓度水平的IL 1β或TNF α诱导培养 2 4小时后均能显著增加HPMC培养液中的PAI 1活性 ,即 0 2 μg/L(IL 1β :q =3 76 ,P <0 0 5 ;TNF α :q =4 91,P <0 0 1) ,2 0 μg/L(IL 1β :q =10 72 ,P <0 0 1;TNF α:q =14 49,P <0 0 1)and 2 0 μg/L(IL 1β :q =2 2 81,P <0 0 1;TNF α:q =2 3 47,P <0 0 1) ,而IL 1β和TNF α对HPMC的诱导效应之间没有显著性差异。结论 前炎症细胞因子在体内可能调节着HPMC释放PAI 1,由此影响着纤维蛋白在胸膜腔内的沉积而向纤维化发展。
Objective To investigate the induction effect of pro-inflammatory cytokines on the release of plasminogen activator inhibitor (PAI 1) from human pleural mesothelial cells (HPMC). Methods Six primary HPMCs exudative pleural effusion were incubated in DMEM / F12 medium in vitro. The effects of proinflammatory cytokines interleukin 1β (IL 1β) and tumor necrosis factor α (TNFα) Effect of dissolution activity. The purity of isolated HPMC was identified by light microscopy, ultrastructure and immunohistochemical staining under electron microscopy. After adding IL 1β or TNFα for 4 h, the third generation of HPMC was cultured for 4 h, and the activity of PAI 1 in HPMC medium Substrate colorimetric assay. Results Compared with the control group, the levels of PAI 1 in HPMC medium were significantly increased after IL 1β or TNFα induction at the following three concentrations for 24 hours: 0 2 μg / L (IL 1β: q = 3 76, P <0.05; TNFα: q = 4 91, P <0.01), 20 μg / L (IL 1β: q = 10 72, P <0.01) , P <0.01) and 20 μg / L (IL 1β: q = 2 2 81, P <0.01); TNFα: q = 2373 There was no significant difference in the induction effect of α on HPMC. Conclusions Proinflammatory cytokines may regulate the release of PAI 1 by HPMC in vivo, thereby affecting fibrin deposition in the pleural cavity and fibrosis.