| Objective:To study the mechanism of liver cancer cell proliferation, apoptosis treated by tanshinoneⅡA, and research the possible mechanism of apoptosis induced by tanshinone. And provide new experimental and theoretical basis for clinical liver cancer treatment.Methods:The HCC cell line SMMC-7721 was used as a model, MTT assay was used to test proliferation of liver cancer treated by tanshinoneⅡA, observe the morphology of SMMC-7721 cells treated by tanshinoneⅡA through light microscopy. The cell cycle and apoptosis of HCC induced by tanshinoneⅡA was tested by Flow cytometric array, western blot was used to research the activation of caspase-3, the shear of PARP protein and the expression of IAP protein XIAP. And RT-PCR was used to test the expression of survivin mRNA.Results:The inhibition of SMMC-7721 cell growth by tanshinone were dose-and time-dependent, And the inhibiting concentration of 50%(IC50) cell proliferation of tanshiinoneⅡA at 24 huors is 2.50 p.g/mL, and 0.46μg/mL for 48 huors. Morphology assay found that SMMC-7721 cells became small and many cell death when treat by tanshinoneⅡA. Through the flow cytometric experiment found that the G1 phase cell was increasing to 63%by control 53.2%, and S/G2/M period cells was significantly reduce when treated by tanshinone II A. The X-linked inhibitor of apoptosis protein(XIAP) was down-regulated, the apoptosis proteins caspase-3 was activative, and PARP protein is been sheard in SMMC-7721 cells when treated by tanshinoneⅡA, But tanshinoneⅡA could not change survivin expression.Conclusion:TanshinoneⅡA could inhibit the growth of HCC through inhibiting cell cycle and inducing apoptosis, and the inhibition effect was dose-and time-dependent. The apoptosis proteins caspase-3 was activative, and PARP protein is been sheard and the expression of XIAP was down-regulated when SMMC-7721 cell was treated with tanshinoneⅡA, but But tanshinoneⅡA could not change survivin expression. |
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