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Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line

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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 μmol/L psoralidin respectively) and up-regulates activities of caspase-3, -8 and -9 in a concentration dependent manner (between 4 to 64 μmol/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 μmol/L (P<0.05 at 16 and 64 μmol/L). Caspase-3 inhibitor (Ac-DEVD-CHO at concentrations between 10 to 20 μmol/L), p53 inhibitor (pifithrin-α at 5 μmol/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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Authors and Affiliations

Authors

Contributions

Yu B and Zhou K designed the experiments; Wang AH, Zhou K, Chai LJ and Liu L performed the experiments; Yu B, Wang AH and Zhou K analyzed data; Yu B and Zhou K drafted manuscript.

Corresponding author

Correspondence to Kun Zhou.

Additional information

Supported by the National Natural Science Foundation of China (No. 81202991) and Tianjin City Application Basis, Cutting-edge Technology Research Program (Tianjin Municipal Science and Technology Commission, No. 13JCYBJC38500)

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Yu, B., Wang, Ah., Zhou, K. et al. Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line. Chin. J. Integr. Med. 25, 757–762 (2019). https://doi.org/10.1007/s11655-016-2251-5

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  • DOI: https://doi.org/10.1007/s11655-016-2251-5

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