【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。更多还原

【Abstract】 Objective To study the effect of the ciglitazone on hepatic cancer cells HepG₂ growth in vivo and its mechanisms.Methods HepH₂ cells（1×10⁶/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 HepG₂ cells 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.更多还原