The study of the therapeutic effect and preliminary mechanism of EGCG on recurrent aphthous ulcer.

To investigate the pro-healing effect of epigallocatechin gallate (EGCG) on mucosal wounds of recurrent aphthous ulcer (RAU) mice and its molecular mechanism. The RAU mouse model was created using chemical cauterization, and ulcerated tissue was collected to observe morphological changes. Network pharmacology identified potential targets and mechanisms. TNF-α and IL-6 levels in ulcer tissues were measured using IHC and ELISA. Western Blotting and RT-qPCR assessed protein and RNA expressions of TLR4, MYD88, NF-κB, and related factors. A CCK8 assay evaluated the effect of drug concentration on cell activity. Finally, molecular docking and CETSA confirmed the association between EGCG and key target molecules. EGCG has been proven to accelerate the healing of ulcers in ICR mice. Meanwhile, EGCG improved the pathologic morphology of the oral mucosa in mice. A network pharmacological analysis of EGCG's impact on RAU may be associated with the Toll-like receptor signaling pathway. Simultaneously, the levels of TNF-α, IL-6, and the expressions of TLR4, MyD88, p-IKB-α, and p-NF-κBP65/NF-κB P65, NF-κB 1 were decreased. The level of IKB-α was elevated, Showing dose dependence. The EGCG-H group showed better results than the positive control group; EGCG was tightly bound to TLR4 and NF-κB p65 target proteins. In conclusion, EGCG promotes the healing of oral ulcers in RAU mice and increases collagen fiber volume fraction in ulcerated skin tissue. The mechanism may be associated with reducing TNF-α and IL-6 expression levels and inhibiting the TLR4/MyD88/NF-κB signaling pathway.