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出 处:《肝胆外科杂志》2005年第5期386-388,共3页Journal of Hepatobiliary Surgery
摘 要:目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂c ig litazone对人肝癌细胞株H epG2体内生长的影响及机制。方法建立裸鼠肝癌动物模型,随机将其分为对照组(A组,10只)和c ig litazone实验组(B组,10只)。B组隔天注射c ig litazone 100μl(100μm o l/L)于瘤内连续15次,对照组同期注射等量生理盐水。1个月后,切除瘤灶,测量瘤灶大小,并检测肿瘤细胞周期素D 1、细胞周期素依赖性激酶抑制p21蛋白及凋亡相关蛋白caspase3的表达。结果c ig litazone治疗后,B组较对照组的生长显著延缓(P<0.05),B组的cyclinD 1较A组明显降低(P<0.05),而其的p21蛋白、凋亡蛋白caspase3表达水平较A组明显升高(P<0.05)。结论c ig litazone能抑制肝癌H epG2细胞的恶性增殖,其机制可能与PPARγ干预细胞周期和细胞凋亡有关。Objective To study the effect of the ciglitazone on hepatic cancer cells HepG2 growth in vivo and its mechanisms. Methods HepH2 cells (1 × 10^6/mouse) were inoculated subcutaneously into 20 nude mice,which were randomly divided into two groups : the control group (group A, n = 10), the ciglitazone treated group (group B, n = 10). The expressions of cyclinD1 ,caspase3 and p21 were analyzed by Western blot. Result The direct injection of ciglitazone into HepG2- induced tumors was able to suppress hepatic cancer growth in nude mice. The expression of cyclinD1 in group B was decreased significantly than that of group A (P〈0.05),the lever of p21 and caspase3 were increased significantly in group B when compared with group A(P〈0.05). Conclusion Ciglitazone could significantly inhibit HepG2cells growth and its mechanism may be due to the fact that It could induce the differentiation of HepG2 cells and induce the apoptosis of HepG2 cells.
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