首页> 中文期刊> 《中国临床保健杂志》 >基于缺氧诱导因子及PI3 K-AKT-mTOR信号通路诱导佐剂关节炎滑膜血管新生的实验观察

基于缺氧诱导因子及PI3 K-AKT-mTOR信号通路诱导佐剂关节炎滑膜血管新生的实验观察

         

摘要

目的 观察佐剂关节炎大鼠滑膜血管PI3K-AKT-mTOR信号通路及缺氧诱导因子(HIF-1α)、血管内皮细胞生长因子(VEGF-A)、滑膜微血管密度(MVD)表达.方法 采用随机数字表法将30只大鼠均分成两组:正常组,模型组,模型组采用弗氏完全佐剂建立佐剂关节炎模型.造模成功后19 d,采用免疫组织化学法检测滑膜血管MVD表达,酶联免疫吸附法检测血清白介素-6(IL-6)、白介素-10(IL-10)、HIF-1α、VEGF-A表达,免疫印迹检测滑膜血管PI3K-AKT-mTOR通路蛋白表达.结果 与正常组比较,模型组大鼠关节炎及MVD计数升高,血清IL-6、VEGF、HIF-1α和滑膜血管磷脂酰肌醇3激酶(PI3K)、蛋白激酶B1(AKT1)、p-AKT1、哺乳动物雷帕霉素靶向蛋白(mTOR)表达显著升高,IL-10降低(P<0.05或P<0.01).结论 PI3K-AKT-mTOR通路过度激活可能是引起滑膜血管新生的原因之一.%Objective To observe the change of PI3K-AKT-mTOR signaling pathway,hypoxia inducible factor (HIF-1α),vascular endothelial growth factor(VEGF)and microvessel density(MVD)of synovial tissue in rats of ad-juvant arthritis.Methods 30 rats were randomly divided into two groups,normal control and model control group.The model control group were established by using Freund′s complete adjuvant.The expression of microvascular density (MVD)were detected using immunohistochemical ninteen days after the modeling.Interleukin(IL)-6,IL-10,HIF-1α and VEGF were detected by enzyme-linked immunosorbent assay.PI3K,AKT1,p-AKT1,mTOR protein were detected by Werstern blotting.Results Compared with normal control group,paw swelling,arthritic index were increased and serum IL-6,VEGF,HIF-1αof serum MVD,PI3K,AKT1,p-AKT1,mTOR of synovial vascular were significantly increased in model control group.There were positive correlation between HIF-1αand MVD,VEGF-A,PI3K and MVD,p-AKT1 pro-tein,and PI3K,p-AKT1 were positively correlated with VEGF-Α,HIF-1α,mTOR were positively correlated with VEGF-A,PI3K,AKT(P<0.05).Conclusion Excessive activation of PI3K-AKT-mTOR pathway might be involved in the synovial angiogenesis in rats with adjuvant arthritis.

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