目的： 探讨神经胶质瘤细胞（A172/U251）与人血管内皮细胞(human brain microvascular endothelial cell, HBMEC)之间STAT3信号通路的交互作用。方法：建立A172、U251细胞与HBMEC的Transwell共培养体系，ELISA检测A172、U251细胞及其分泌因子VEGF对HBMEC分泌IL-6的影响，Western blotting检测HBMEC与A172/U251细胞共培养30 min时HBMEC及其分泌因子IL-6对A172/U251细胞STAT3蛋白及其磷酸化状态p-STAT3的影响，CCK-8、Transwell侵袭实验分别检测HBMEC及其分泌因子IL-6对A172/U251细胞增殖和侵袭的影响。结果：VEGF(50 ng/ml) 组和共培养组（HBMEC分别和A172，U251细胞共培养） HBMEC的IL-6的表达量明显高于对照组(P<0.01)。共培养30 min时，A172/U251细胞的IL-6(50 ng/ml)组、共培养组及（共培养+AZD1480）组的STAT3/p-STAT3蛋白的表达明显高于对照组(P<0.01)，（共培养+AZD1480）组的胶质瘤细胞STAT3/p-STAT3蛋白的表达能力显著低于共培养组(P<0.01)。IL-6(50 ng/ml)组，共培养组及（共培养+AZD1480）组的A172/U251细胞增殖及侵袭能力明显高于对照组(P<0.01)，（共培养+AZD1480）组的细胞增殖及侵袭能力显著低于共培养组(P<0.01)。结论：神经胶质瘤细胞与人脑微血管内皮细胞之间存在信号交互作用，且与JAK2/STAT3信号通路密切相关。

Objective:To explore the role ofSTAT3 signaling pathway in the interaction of glioma cells and human brain microvascular endothelial cells (HBMEC). Methods: The secretion of IL-6 from HBMEC co-cultured with VEGF，A172, or U251 cells by Elisa. Immunoblotting was performed to examine STAT3 and its phosphorylation status inglioma cells after exposed to IL-6(50 ng/ml), co-cultured with the endothelial cells, orHBMEC+AZD1480. CCK-8 and Transwell assays were used to measure the effect of IL-6 (50 ng/ml), HBMEC, and HBMEC+AZD1480 on the proliferation and invasion of glioma cells A172 and U251. Results: Glioma cells and VEGF promoted the secretion of the IL-6 bythe endothelial cells(P<0.01). The level of pSTAT3 in A172 and U251 was significantly increased after exposed to IL-6， HBMEC， or HBMEC+AZD1480 (P<0.01). Moreover, AZD1480 reduced STAT3 phosphorylationin A172 and U251 co-cultured with HBME(P<0.01). IL-6 (50ng/ml) and co-culturing with the endothelial cells enhanced the growth and invasion of the glioma cells(P<0.01), where as AZD1480 suppressed the growth and invasion of the A172 and U251 cells (P<001). Conclusion: STAT3 activation is involved in the interaction between glioma cells and the human brain microvascular endothelial cells.

国家自然科学基金资助项目（No. 81160312）