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| Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line |
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| KeyWord:psoralidin, apoptosis, HepG2, mitochondria, p53, cyclosporin A |
| Author Name | Affiliation | E-mail | | YU Bin, WANG An-hong | | | | ZHOU Kun | 1. Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin (300193), China
3. Department of pharmacy, Gansu Provincial Hospital, Lanzhou (731600), China
2. Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin (300193), China
5. College of Pharmacy, Henan University, Kaifeng, Henan Province (475004), China | z.k.ken@263.net | | CHAI Li-juan | | |
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| Abstract: |
| Objective: To test the role of psoralidin in human liver cancer HepG2 cells in vitro. Methods: Cell viability was assessed by methylthiazolyldiphenyl-tetrazolum bromide assay and apoptotic cells were labeled by annexin V then sorted by flow cytometry. Protein expressions of caspase-3, caspase-8, caspase-9, Bax, Bid, Bcl-2, Bcl-xL and p53 were examined by western blot while activity of caspase-3, -8 and -9 were also determined. Results: Psoralidin reduces cell viability greatly in a time dependent manner (64%, 40%, 21%, 12% at 2, 6, 24 and 48 h treatment with 64 μ mol/L psoralidin respectively) and up-regulates activities of caspase-3, -8 and -9 in a concentration dependent manner (between 4 to 64 μ mol/L). Psoralidin also increases the expression of pro-apoptosis genes Bax, Bid and p53 while decreases the expression of pro-survival genes Bcl-2 and Bcl-xL, both in a concentration dependent manner between 4 and 64 μ mol/L (P<0.05 at 16 and 64 μ mol/L). Caspase-3 inhibitor (Ac-DEVD-CHO at concentrations between 10 to 20 μ mol/L), p53 inhibitor (pifithrin-α at 5 μ mol/L) and cyclosporin A can attenuate the apoptotic effect of psoralidin. Conclusion: The cytotoxic role of psoralidin might work through both intrinsic and extrinsic apoptotic pathway. |
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