ArticleThe Journal of international medical research2018
Tetrandrine inhibits the proliferation and cytokine production induced by IL-22 in HaCaT cells.
Article in The Journal of international medical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Enhancing secondary metabolite accumulation in medicinal plants to improve immunomodulatory activity.Frontiers in pharmacology · 2026Review
- Therapeutic potential of recombinant IL-22BP in psoriasis: suppression of IL-22/STAT3 signaling in mice.AMB Express · 2025Article
- Single-Cell Sequencing and Machine Learning Integration to Identify Candidate Biomarkers in Psoriasis:Journal of inflammation research · 2024Article
- Yangxin granules alleviate doxorubicin-induced cardiotoxicity by suppressing oxidative stress and apoptosis mediated by AKT/GSK3The Journal of international medical research · 2020Article
- Anticancer Activity of Tetrandrine by Inducing Apoptosis in Human Breast Cancer Cell Line MDA-MB-231 In Vivo.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effect of tetrandrine (Tet) on HaCaT cell proliferation and cytokine expression induced by interleukin (IL)-22, and to investigate the underlying mechanism.
methodsThe half maximal inhibitory concentration (IC50) and antiproliferation effects of Tet on IL-22-treated HaCaT cells were analysed by MTT assay. Signal transducer and activator of transcription 3 ( STAT3) expression was measured by reverse transcription plus real-time quantitative polymerase chain reaction (qPCR) and by Western blot. Phosphorylated (p)-STAT3 levels were also measured by Western blot. Cytokine production by HaCaT cells was analysed by enzyme-linked immunosorbent assay (ELISA) following administration of IL-22 and/or Tet.
resultsTet displayed a dose-dependent inhibitory effect on HaCaT cell proliferation and reduced the phosphorylation level of STAT3 induced by IL-22, without affecting STAT3 mRNA and protein levels. Furthermore, co-incubation with Tet significantly down-regulated HaCaT cell production of tumour necrosis factor (TNF)-α, IL-1β, IL-6, IL-20 and chemokine (C-C motif) ligand 20 (CCL20) induced by IL-22.
conclusionsTet inhibits proliferation and cytokine production in HaCaT cells, and the process may involve the inhibition of STAT3 phosphorylation.
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Registered trials
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