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目的 观察肺炎衣原体感染对人血管内皮细胞迁移的影响,探讨黄连素对其干预作用及作用机制.方法 体外成功培养肺炎衣原体AR-39株后,感染不同浓度黄连素(0、100、150及200 mmol/L)预处理的内皮细胞,在感染后24、48及72 h,创伤修复实验、Transwell实验观察内皮细胞迁移的变化,逆转录聚合酶链反应和酶联免疫吸附法检测内皮细胞中信号蛋白PI3K mRNA表达水平和酶活性.结果 与正常对照组比较,肺炎衣原体感染组内皮细胞于24、48及72 h迁移量均明显增加(P<0.01),且PI3K mRNA表达水平显著升高,酶活性亦明显增强(P<0.01);与肺炎衣原体感染组比较,PI3K抑制剂Lγ294002组内皮细胞迁移量明显减少(P<0.01),PI3K mRNA表达水平明显降低,酶活性也明显减弱(P<0.01);与肺炎衣原体感染组比较,黄连素中剂量组和高剂量组内皮细胞迁移量均明显下降(P<0.01),PI3K mRNA表达水平和酶活性均明显降低(P<0.01),且PI3K mRNA表达水平和酶活性均与细胞迁移抑制程度呈正相关(r分别为0.841和0.832,P<0.01).结论 肺炎衣原体感染可能是通过激活PI3K诱导内皮细胞迁移;黄连素可拮抗肺炎衣原体感染诱导的内皮细胞迁移,其机制可能与黄连素下调PI3K表达及抑制PI3K活化有关.“,”Aim To observe the effects of Chlamydia pneumoniae infection on migration of endothelial cells,to investigate the interventive effect of Berberine on Chlamydia pneumoniae induced-endothelial cell migration and to explore its possible mechanism. Methods Endothelial ceils pretreated with Berberine at different concentration(0,100,150 and 200 mmol/L)were infected by Chlamydia pneumoniae AR-39 in vitro.At 24,48 and 72 h after Chlamydia pneumoniae infection,the wound healing assay and Transwell assay were performed to observe the effects of Berberine on migration of endothelial cells.The mRNA expression and enzymatic activity of PDK were detected by RTPCR and ELISA at the corresponding time point. Results Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K increased significantly at 24,48 and 72 h after Chlamydia pneumoniae infection in comparison with the control group (P<0.01).Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K decreased markedly after administration of the PI3K inhibitor of LY294002 compared with the Chlamydia pneumoniae infection group(P<0.01).Migration of endothelial cells,the mRNA expression and enzymatic activity of PI3K decreased markedly after administration of the middle-dose and high-dose Berberine compared with the Chlamydia pneumoniac infection group(P<0.01),and migration of endothelial cells was positively correlated with the mRNA expression(r_1)and enzymatic activity of P13K(r_2)(r_1=0.841,r_2 =0.832,P<0.01). Conclusions Chlamydia pneumoniae may induce endothelial cell migration via the activation of PI3K. Berberine can antagonize Chlamydia pneumoniae induced-endothelial cell migration possibly through downregulating the PI3K mRNA expression and inhibiting the activation of PI3K.