The Effect Of PPAR Gamma Agonist On Proliferation In The Human Hepatoma Cell Line HepG2 And Approach To The Mechanism

Purpose: The aim of this article is to observe the effect of PPAR gamma agonist Rosiglitazone on proliferation in the human hepatoma cell line HepG2 in vitro and approach to the mechanism. Methods: MTT assay was used to detect the proliferative influence of different concentration of Rosiglitazone (10μmol/L, 30μmol/L, 50μmol/L, 100μmol/L, respectively) on HepG2 cells. The ratio of apoptosis and the distribution in cell cycle were detected by FCM. The expression of PPARγ, PTEN, Bax, Bcl-2 and Caspase-3 in HepG2 cells were semi-quantitated by immunohistochemistry. TUNEL and transmission electron microscope were applied to observe the apoptotic morphological changes. Results: Activation of PPAR gamma by Rosiglitazone caused a marked growth inhibition in a dose and time dependent manner in HepG2 cells. Cell cycle was arrested in G0/G1-phase. The expression of PTEN, Bax and Caspase-3 protein were up-regulated, but Bcl-2 was down-regulated. Apoptotic cells were seen in Rosiglitazone-treated group by TUNEL and transmission electron microscope. Conclusion: PPAR gamma agonist Rosiglitazone could inhibit HepG2 cell growth, one of the main mechanisms is promoting cell apoptosis, which may be related with the regulation of protein expression of Bax, Bcl-2 and Caspase-3.