ArticleChinese journal of integrative medicine2019
Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line.
Article in Chinese journal of integrative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Psoralidin inhibits stemness-associated characteristics in cervical cancer cells via modulation of Oct4/Sox2 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Phytochemical basis and antitumor mechanisms ofFrontiers in immunology · 2026Review
- Yin/Yang associated differential responses to Psoralea corylifolia Linn. In rat models: an integrated metabolomics and transcriptomics study.Chinese medicine · 2023Article
- Protective effects and mechanisms of psoralidin against adriamycin-induced cardiotoxicity.Journal of advanced research · 2022Article
- Antioxidant activity of olive flounder (Journal of food science and technology · 2022Article
- A review of alpha-glucosidase inhibitors from plants as potential candidates for the treatment of type-2 diabetes.Phytochemistry reviews : proceedings of the Phytochemical Society of Europe · 2022Review
- Pharmacological Activities of Psoralidin: A Comprehensive Review of the Molecular Mechanisms of Action.Frontiers in pharmacology · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo test the role of psoralidin in human liver cancer HepG2 cells in vitro.
methodsCell 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.
resultsPsoralidin 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.
conclusionThe cytotoxic role of psoralidin might work through both intrinsic and extrinsic apoptotic pathway.
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