中文摘要：

目的 探讨CXCL8/PI3K-Akt信号转导通路在缺氧诱导的人脑胶质瘤细胞株U87MG和U251血管生成拟态中的作用。方法 用氯化钴（Co Cl2）模拟缺氧环境,将人脑胶质瘤细胞株U87MG和U251置中培养。分别加入PI3K-Akt信号通路激动剂CXCL8及PI3K-Akt信号通路抑制剂LY294002干预48 h,体外成管实验检测各组细胞成管能力;Western印迹检测各组Akt、P-Akt蛋白的表达情况。结果 缺氧可导致U87MG细胞和U251细胞形成的管腔样结构明显增加,Akt蛋白的磷酸化活化表达显著增加（P〈0.05）。加入CXCL8干预可使管腔样结构直径进一步增长,而加入LY294002干预48 h则可使其管腔样结构在数量和直径上显著少于缺氧组（P〈0.05）。CXCL8能够有效激活Akt磷酸化,LY294002则显著抑制其磷酸化活化（P〈0.05）,而总Akt蛋白表达无差异（P〉0.05）。结论 CXCL8/PI3K-Akt信号转导通路在缺氧诱导的人脑胶质瘤细胞株U87MG和U251血管生成拟态中发挥重要的促进作用,可望成为胶质瘤治疗有效靶点。

英文摘要：

Objective To study the roles of CXCL8/PI3K-Akt signaling pathway in vascular mimicry induced by hypoxia of human glioma cell. Methods The chemical hypoxia was induced by incubation of U87MG cells and U251 cell with cobalt chloride. After the two cells were treated with CXCL8 （the activator of PI3K/Akt）and LY294002 （the inhibitor of PI3K/Akt）for 48 h, the tube formation of tumor cells were tested by transwell chamber test and vascular mimicry experiment. Western blot assay was employed to determine the expressions of Akt and p-Akt. Results The formed tubes of U87MG cells and U251 cells were significantly increased by incubated with cobalt chloride,either did the expression level of p-Akt. Compared to hypoxia group, there were more formed tubes after CXCL8 treatment, while less formed tubes after LY294002 treatment. Western blot indicated that the expression of p-Akt at protein level was decreased（ P〈0. 05 ） ,while STAT3 protein had no difference among each group（P〉0.05）. Conclusions CXCL8/PI3K-Akt signaling pathway plays an important roles in vascular mimicry induced by hypoxia of human glioma cells in vitro, so it could be expected as a potential target for the treatment of glioma.