The Effect of Wogonin on the Inflammatory Response in an M5-Induced Psoriasiform HaCaT Cell Model by Regulating the STING/NF-κB Pathway

This article aims to investigate the effect of WOG (wogonin) on the inflammatory response in an M5-induced psoriasiform HaCaT cell model and the role of the STING/NF-κB pathway in this process. HaCaT cells were randomly divided into the NC group, the M5 (five proinflammatory cytokines) group, the M5+WOG group, the M5+STING inhibitor (H-151) group, and the M5+WOG+STING agonist (SR-717) group. Cell proliferation and apoptosis were detected by CCK-8, EdU staining and flow cytometry, respectively. Immunofluorescence was used to detect indicators related to cell barrier function damage. qPCR and ELISA were respectively used to detect the expression levels of characteristic factors of inflammatory response and psoriasis. Western blot was used to measure the proteins related to the STING/NF-κB signaling pathway. Compared with the NC group, the proliferation activity and proliferation rate of HaCaT cells, the relative expression levels of IL-6, IL-8 and TNF-α mRNA, the contents of S100A7, S100A8 and DEFB4, the ratios of p-STING/STING, p-TBK1/TBK1 and p-p65/p65 in the M5 group were all significantly increased, while the apoptosis rate, the positive rates of ZO-1, Occludin and E-cadherin were all significantly decreased (P<0.05). Treatment with either WOG or the STING inhibitor H-151 effectively reversed the aforementioned effects induced by M5 (P<0.05). Notably, the STING agonist SR-717 partially counteracted the protective effects of WOG, indicating that the therapeutic efficacy of WOG was dependent on the inhibition of the STING/NF-κB pathway (P<0.05). WOG effectively suppresses the proliferation of M5-induced psoriasiform HaCaT cells promotes their apoptosis, repairs the damage to the cell barrier function, and alleviates the inflammatory response by inhibiting the STING/NF-κB signaling pathway

CSTR: 32200.14.cjcb.2026.02.0013