Tanshinone II-A Induced Apoptosis of HepG2: Involvement of p53, Bcl-2 and Bax

Background: Tanshinone was thought to be a potential antitumor drug. In this study, we investigated the apoptosis of hepatoma HepG2 induced by Tanshinone II-A as well as the involved molecules. Methods: The inhibitory effects on cell proliferation of Tanshinone II-A were assessed by MTT method. DNA fragmentation was evaluated by agarose gel electrophoresis. Cell cycle and apoptotic rates were quantified by flow cytometry (FCM). The expressions of p53, Bcl-2, Bax genes were determined by semi-quantitative RT-PCR. Results: Tanshinone II-A significantly inhibited the proliferation rate of human hepatoma HepG2 cells in doseand time-dependent manner. The semi-inhibitory concentration (IC50) was 7.4 μg/ml, 1.9 μg/ml, 0.6 μg/ml for 24, 48, and 72 h respectively. DNA fragmentation in agarose gel revealed series of DNA ladder, which indicated the degradation of genomic DNA induced by apoptosis. Flow cytometry showed that hepatoma HepG2 cells were block in G0/G1 phase and the apoptotic rate elevated significantly after treatment with Tanshinone II-A. In addition, semi-quantitative RT-PCR showed that p53 and Bax increased significantly while Bcl-2 decreased significantly in HepG2 treated with Tanshinone II-A. Conclusion: Tanshinone II-A could inhibit proliferation and induce apoptosis of the human hepatoma HepG2 cells. p53, Bcl-2 and Bax might be involved in this process.