Platycodin D Alleviates High-Glucose-Aggravated Inflammatory Responses in Oral Mucosal Cells by PI3K/mTOR Pathway

Abstract

Oral mucosal diseases account for an increasing proportion of hμMan diseases. Among the many common risk factors that cause oral diseases and systemic diseases, dietary factors, especially high sugar, are particularly prominent. Exhibiting therapeutic potential in treating certain inflammation-related diseases, platycodin D (PD) has been known to possess anti-inflammatory benefits in cases of cytokine-induced inflammation, a fact that has been widely docμMented. However, there are few studies about PD in the oral mucosal disease. Investigating the effect of PD on high-glucose (HG)-induced inflammatory responses in oral mucosal cells was the endeavor of this study. The results revealed that HG induced cell mortality, promoted activity of inflammatory factor (TNF-α, IL-1β, IL-6, and IL-8), and increased ROS production in oral mucosal cells. Interestingly, PD obviously alleviated HG-induced oral mucosal cells inflammatory response. Simultaneously, the expressions of PI3K and mTOR were inhibited by PD. In addition, the activation of PI3K and mTOR decreased the protective effect of PD on oral mucosal cells. To conclude, the PI3K/mTOR signaling pathway was found to be inactivated, thereby restraining the activation of the full immune cell by inhibition of the pro-inflammatory cytokines, as revealed by the results indicating the prevention of the HG-induced inflammation response by PD.