PPARγ配体对人肺癌细胞95-D增殖的影响及机制探讨

Effect and mechanism of PPAR-γ ligand on human lung cancer 95-D cell proliferation and apoptosis

目的观察过氧化物酶体增殖体激活受体γ(PPARγ)的合成配体曲格列酮(TGZ)和天然配体15-脱氧前列腺素J2(15-PGJ2)对肺癌95-D细胞增殖活性及凋亡的影响,并探讨其机制。方法将对数生长期的95-D细胞分为TGZ组、15-PGJ2组、对照组,分别加入500μl的TGZ溶液、15-PGJ2溶液、DMSO混合溶液培养;采用MTT法检测95-D细胞的增殖能力,采用流式细胞仪检测95-D细胞凋亡率和细胞周期变化,采用免疫细胞化学法检测95-D细胞中的PPARγ。结果与对照组比较,TGZ、15-PGJ2组95-D细胞增殖抑制率显著增加(P均<0.01),且存在时相性;95-D细胞凋亡率增加,S期细胞比例升高,G1期细胞比例降低;95-D细胞中PPARγ表达水平增加。结论PPARγ配体TGZ、15-PGJ2可抑制95-D细胞增殖,诱导其凋亡;该作用与PPARγ表达增加有关。

Objective To observe the effect of PPAR-γ ligand on human lung cancer 95-D cell proliferation and apoptosis,and explore its mechanism.Methods 95-D cells were cultured in vitro and divided into control group,TGZ group（cultured with troglitazone）and 15-PGJ2 group（cultured with 15-PGJ2）.Cell proliferation inhibition rate of 95-D was detected by MTT assay,apoptosis and cell cycle kinetics was detected by flow cytometry and expression of PPAR-γ in 95-D cell was detected by immunohistochemistry.Result The proliferation inhibition rate,apoptosis rate and PPARγ expression of 95-D cells in TGZ and 15-PGJ2 groups were increased.Conclusion PPAR-γ ligands can induce apoptosis of 95-D cell and inhibit its proliferation in vitro.The mechanism may be mediated by increasing the expression of PPAR-γ.