Conclusions
Tet inhibits proliferation and cytokine production in HaCaT cells, and the process may involve the inhibition of STAT3 phosphorylation.
Methods
The 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.
Objective
To investigate the effect of tetrandrine (Tet) on HaCaT cell proliferation and cytokine expression induced by interleukin (IL)-22, and to investigate the underlying mechanism.
Results
Tet 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. Conclusions: Tet inhibits proliferation and cytokine production in HaCaT cells, and the process may involve the inhibition of STAT3 phosphorylation.