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PPARγ配体Ciglitazone对人胃癌MGC803细胞增殖的影响及其机制[J]. 肿瘤防治研究, 2008, 35(03): 164-168. DOI: 10.3971/j.issn.1000-8578.1841
引用本文: PPARγ配体Ciglitazone对人胃癌MGC803细胞增殖的影响及其机制[J]. 肿瘤防治研究, 2008, 35(03): 164-168. DOI: 10.3971/j.issn.1000-8578.1841
Effect of PPARγ Ligand Ciglitazone on Human Gastric Carcinoma MGC803 Cells Proliferation and Its Mechanism[J]. Cancer Research on Prevention and Treatment, 2008, 35(03): 164-168. DOI: 10.3971/j.issn.1000-8578.1841
Citation: Effect of PPARγ Ligand Ciglitazone on Human Gastric Carcinoma MGC803 Cells Proliferation and Its Mechanism[J]. Cancer Research on Prevention and Treatment, 2008, 35(03): 164-168. DOI: 10.3971/j.issn.1000-8578.1841

PPARγ配体Ciglitazone对人胃癌MGC803细胞增殖的影响及其机制

Effect of PPARγ Ligand Ciglitazone on Human Gastric Carcinoma MGC803 Cells Proliferation and Its Mechanism

  • 摘要: 目的探讨PPARγ配体Ciglitazone对人胃癌MGC803细胞增殖的影响及其机制。方法RTPCR检测MGC803细胞PPARγ mRNA。MTT及流式细胞术检测Ciglitazone对MGC803细胞增殖及凋亡的影响。相差倒置显微镜和Hoechst33342染色观察凋亡的形态学变化。免疫组化和流式细胞术检测PPARγ、Bcl-2、Bag-1及Bax蛋白表达和变化。结果PPARγ配体Ciglitazone(5、10、20和50μmol/L)可抑制MGC803细胞增殖和诱导其凋亡,增殖的抑制和凋亡的诱导有平行性,且有浓度和时间依赖性。随20μmol/L Ciglitazone作用时间的延长,MGC803细胞的PPARγ mRNA及蛋白表达、Bax蛋白表达及Bax/Bcl-2蛋白的比值升高,Bcl-2和Bag-1蛋白表达降低。结论Ciglitazone可能主要通过激活PPARγ抑制人胃癌MGC803细胞增殖和诱导其凋亡。Bax蛋白表达和Bax/Bcl-2蛋白表达比值升高,Bcl-2和Bag-1蛋白表达降低在Ciglitazone诱导人胃癌MGC803细胞凋亡中起重要作用。提示Ciglitazone可能对治疗胃癌有效。

     

    Abstract: Objective  To investigate effect of peroxisome proliferator2activated receptorγ( PPARγ) ligand Ciglitazone on proliferation of human gast ric carcinoma MGC803 cells and it s mechanism. Methods  To examine PPARγmRNA of MGC803 cells by RT2PCR. To examine effect of PPARγligand Ciglitazone on MGC803 cells proliferation and apoptosis by MTT and Flow Cytomet ry. To examine morphological change of apoptosis by phase cont rast microscope and Hoechst33342 staining. To examine the expression and change of PPARγ,Bcl22, Bag21 and Bax protein of MGC803 cells by immunohistochemist ry and Flow Cytomet ry. Results  Ciglitazone (5μmol/ L 、10μmol/ L 、20μmol/ L and 50μmol/ L) inhibited proliferation and induced apoptosis of MGC803 cells and apoptosis is parallel to proliferation inhibition in MGC803 cells, which were dose2 and time2dependent . PPARγmRNA and protein expression, Bax protein expres2 sion and Bax protein over Bcl22 protein ratio were enhanced and both Bcl22 and Bag21 protein expression were decreased with prolonged time following 20μmol/ L Ciglitazone t reatment in MGC803 cells. Conclu2 sion  Ciglitazone may inhibit proliferation and induce apoptosis in human gast ric carcinoma MGC803 cells via activating PPARγ. Elevated Bax protein expression and Bax protein over Bcl22 protein ratio and de2 creased Bcl22 and Bag21 protein expression may play an important role during apoptosis of human gast ric carcinoma MGC803 cells induced by Ciglitazone, which suggest that Ciglitazone may effective to t reat gas2 t ric carcinoma.

     

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