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

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.