Yangyin Shengji Powder inhibits inflammation and promotes the wound-healing in oral ulcers through regulating SIRT1/NF-κB p65 signaling pathway.

Yangyin Shengji Powder (YYSJS) has been empirically used for the treatment of oral ulcers, but its underlying pharmacological mechanism remains unclear. In this study, we investigated the therapeutic effects and potential mechanism of YYSJS in both in vivo and in vitro models of oral ulcer. A rat model of chemotherapy-associated oral ulcer was established by intraperitoneal injection of 5-fluorouracil followed by local NaOH cauterization, while an in vitro inflammatory model was induced by lipopolysaccharide stimulation of rat oral mucosal fibroblasts. Serum collected from rats after intragastric administration of YYSJS (termed YYSJS-containing serum) was applied to treat lipopolysaccharide-challenged fibroblasts. The results showed that YYSJS significantly accelerated ulcer healing, reduced wound area, and improved histopathological changes in the oral mucosa. YYSJS also restored the balance between pro-inflammatory and anti-inflammatory cytokines, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6, along with increased IL-10 expression in ulcer-bearing rats. In addition, the expression levels of epidermal growth factor and epidermal growth factor receptor in ulcer tissues were markedly elevated after YYSJS treatment. In LPS-stimulated fibroblasts, YYSJS-containing serum suppressed the release of pro-inflammatory cytokines, enhanced IL-10 secretion, and promoted cell proliferation, as demonstrated by CCK-8 and colony formation assays. Mechanistically, YYSJS upregulated SIRT1 protein expression and inhibited the nuclear translocation of NF-κB p65 both in vivo and in vitro. These findings suggest that YYSJS promotes oral ulcer healing by alleviating inflammation and enhancing cell proliferation, possibly through regulation of the SIRT1/NF-κB p65 signaling pathway.