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目的观察经动脉插管注入血管生成抑制剂YH-16和化疗栓塞联合应用对大鼠移植型肝癌的抑制作用。方法取大鼠乳腺癌细胞株(Walker 256)转染至肝脏的荷瘤大鼠动物模型,随机分成4组,每组12只。各组具体治疗方案如下:A组:经肝动脉缓慢灌注生理盐水;B组:经肝动脉缓慢灌注超液化碘油;C组:经肝动脉缓慢灌注丝裂霉素+超液化碘油;D组:经肝动脉灌注丝裂霉素+超液化碘油+YH-16,术后10 d观察各组大鼠原发肿块大小并采用免疫组化方法检测肝肿瘤血管内皮生长因子(VEGF)的表达和肿瘤微血管密度(MVD)。结果B、C、D 3组肝肿瘤的体积均小于A组(均P<0.05),而D组又小于B、C组(均P<0.05)。B组VEGF的表达以及MVD计数明显大于A组(P<0.05),A、C2组组间比较差异无统计学意义(P>0.05)。D组VEGF的表达及MVD计数均明显小于A、C2组(均P<0.05)。结论经肝动脉灌注血管生成抑制剂YH-16联合经动脉化疗栓塞能抑制移植型肝癌的生长,并对肿瘤组织的微血管数目和VEGF的表达具有显著的抑制作用。
Objective To observe the inhibitory effect of intra-arterial infusion of angiogenesis inhibitor YH-16 combined with chemoembolization on transplanted hepatocellular carcinoma in rats. Methods The animal model of tumor-bearing rats transfected with rat breast cancer cell line (Walker 256) was randomly divided into 4 groups (n = 12). Group A: slow infusion of saline through the hepatic artery; Group B: slow infusion of liquefied iodized oil via the hepatic artery; Group C: slow infusion of mitomycin + liquefied lipiodol via the hepatic artery; D Group: The rats were perfused with mitomycin + liquefied lipiodol + YH-16 via hepatic artery. The size of the primary tumor in each group was observed 10 days after operation. Immunohistochemistry was used to detect the expression of vascular endothelial growth factor Expression and tumor microvessel density (MVD). Results The volume of liver tumors in groups B, C and D were smaller than those in group A (all P <0.05), while those in group D were less than those in groups B and C (all P <0.05). The expression of VEGF and MVD in group B were significantly higher than those in group A (P <0.05). There was no significant difference between group A and group C2 (P> 0.05). The expression of VEGF and MVD in group D were significantly lower than those in group A and C2 (all P <0.05). Conclusion The hepatic artery perfusion of angiogenesis inhibitor YH-16 combined with transarterial chemoembolization can inhibit the growth of transplanted hepatocellular carcinoma and significantly inhibit the number of microvessels and the expression of VEGF in tumor tissue.