肠复康抑制人大肠癌HT29裸小鼠移植瘤细胞增殖的机制

Mechanism of Chang-fu-kang on the inhibition of proliferation of transplant tumor cells in the nude mice by human large intestine cancer HT29 cells

目的探讨肠复康抑制人大肠癌HT29裸小鼠移植瘤细胞增殖的机制。方法建立人大肠癌HT29癌细胞株裸小鼠皮下移植瘤模型,免疫组化染色结合图像分析系统半定量检测移植瘤细胞KI-67阳性细胞数、血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)、血管内皮生长因子受体(fetalliverkinase-1,FLK-1)和转化生长因子β1(transforminggrowthfactorbeta1,TGF-β1)的积分光密度(integraopticaldensit,IOD),并使用逐步引入剔出模型进行多元线性回归分析。结果与模型组比,肠复康组和西药组均使移植瘤KI-67阳性细胞数明显减少(P<0.001),同时能显著降低瘤细胞VEGF、FLK-1和TGF-β1的含量(P<0.05～0.001);回归分析结果,移植瘤KI-67阳性细胞数与瘤细胞VEGF和FLK-1含量呈明显正相关(前者r=0.802,P<0.001;后者r=0.668,P<0.001)。结论肠复康能抑制人大肠癌HT29裸小鼠移植瘤细胞增殖,其机制之一可能是减少瘤细胞的VEGF、FLK-1和TGF-β1的生成,特别是减少VEGF和FLK-1的生成。

Aim To investigate the mechanism of Chang fu kang on the inhibition of proliferation of transplant tumor cells in nude mouse by human large intestine cancer HT29 cells.Methods HT29 nude mouse were randomly divided into three groups: model group of 8 mouse, Chang fu kang group of 7 mouse and western medicine group of 8 mouse. The number of positive Ki 67 cells, integra optical densit(IOD) of vascular endothelial growth factor(VEGF) , fetal liver kinase 1(FLK 1) and transforming growth factor beta 1(TGF β1) were semi quantitatively examined by immunohistochemical stain methods combined with image analysis system. Multiple linear regression analysis was conducted to analyze the results with stepwise method.Results In comparison with the model group, the number of positive Ki 67 cells and the content of VEGF, FLK 1 and TGF β1 were significantly reduced (P< 0.001) in the Chang fu kang and western medicine groups (P< 0.05-0.001).The number of the positive Ki 67 cells was significantly correlated to the content of VEGF (r=0.802,P< 0.001) and FLK 1(r=0.668, P< 0.001).Conclusion The proliferation of the transplant tumor cells in nude HT29 mouse was inhibited by Chang fu kang, and one of its mechanisms was possible to reduce the production of VEGF, FLK 1 and TGF β1, particularly to reduce that of VEGF and FLK 1.