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目的研究 p38信号传导通路在血管内皮细胞生长因子(vascular endothdial growth factor,VEGF)诱导肝癌细胞超微结构变化中的作用.方法采用扫描电子显微镜观察 VEGF 以及预先用 SB203580特异性阻断 p38MAPK 信号传导通路后 VEGF 诱导肝癌细胞HepG_2形态学改变.结果扫描电镜显示肝癌细胞呈梭形,表面有细而稀疏的突起,VEGF 诱导后肝癌细胞成椭圆形,细胞表面伪足增多、变粗.阻断 p38MAPK 信号通路后,可抑制 VEGF 诱导的肝癌细胞表面伪足增多、变粗,促进肝癌细胞融合.结论 VEGF 通过 p38MAPK 信号通路诱导肝癌细胞伪足增多、变粗,降低细胞间粘附作用.
Objective To investigate the role of p38 signal transduction pathway in the ultrastructural changes of hepatoma cells induced by vascular endothelial growth factor (VEGF). Methods The VEGF was observed by scanning electron microscopy and the p38MAPK signaling pathway was specifically blocked by SB203580 in advance. After VEGF induced hepatoma cell HepG_2 morphological changes. The results of scanning electron microscopy showed that the hepatoma cells were fusiform, the surface has thin and sparse protuberances, VEGF induced hepatoma cells into oval-shaped, cell surface pseudopodia increased, thicker. Block p38MAPK signal After the pathway, it can inhibit the increase and thickening of pseudopodia on the surface of hepatocellular carcinoma cells induced by VEGF, and promote the fusion of hepatocellular carcinoma cells. Conclusion VEGF can induce pseudopodia of liver cancer cells through the p38MAPK signaling pathway to increase, thicken, and reduce the intercellular adhesion.