Apoptosis Of Human Hepatoma HepG2 Cells Induced By Tanshinone ⅡA In Vitro

Primary carcinoma of the liver is one of the most ordinary malignancy in china, with pathologic characters of unconventional proliferation and invasion of other tissues and organs. Apoptosis is an active process adjusted by many factors to keep stabilization of body. Once apoptosis is inhibited, excessive, damaged and cancerated cells can not be cleared, so the tumor will happen.Tanshinone IIA is one of the major lipophilic components of Salvia miltiorrhiza Bunge (known as Danshen in Chinese), participating in manifold biochemical reactions for its nature of oxidation-reduction and it is mostly used in arthritis and cardiovascular diseases. Recent studies have indicated that Tan IIA not only inhibits inflammation and oxidation, but also has obvious effect of anti-tumor. And the study was designed to investigate the apoptosis effects and mechanisms of TanshinoneⅡA-induced cell death in human hepatoma HepG2 cells.Method: Human hepatoma HepG2 cells were treated by TanshinoneⅡA. The inhibitory effect on cell proliferation was assayed by MTT. DNA fragmentation was evaluated by agarose gel electrophoresis. The expressions of p53, Bcl-2, Bax were assayed by reverse transcription-polymerase chain reaction (RT-PCR). Cell cycle and apoptotic rate were quantified by flow cytometry (FCM).Result: TanshinoneⅡA inhibited the proliferation of human hepatoma HepG2 cells depending on dose and time manners. The semi-inhibitory concentration (IC50) was 7.4μg/ml, 1.9μg/ml, 0.6μg/ml for 24, 48, 72h. DNA ladder was shown in agarose gel electrophoresis. TanshinoneⅡA could strengthen the expressions of p53 and Bax, decline the expression of Bcl-2 at the same time. The human hepatoma HepG2 cells treated by TanshinoneⅡA were block in G1 phase and apoptotic rate rose up.Conclusion: TanshinoneⅡA could inhibit proliferation and induce apoptosis of the human hepatoma HepG2 cells through the pathway of p53, Bcl-2 and Bax.