Berberine suppresses bone loss and inflammation in ligature-induced periodontitis through promotion of the G protein-coupled estrogen receptor-mediated inactivation of the p38MAPK/NF-κB pathway

This study aimed to explore the protective actions of berberine on inflammation, and alveolar bone loss in ligature-induced periodontitis, as well as its mechanism of action Micro-computed tomography was conducted to analyze the alveolar bone loss, and hematoxylin and eosin staining was carried out to observe the histopathological changes and inflammation status. Furthermore, enzyme linked immunosorbent assay (ELISA) was conducted to evaluate the levels of TNF-α, IL-1β, and IL-10, as well as western blots to determine the levels of GPR30 and the activity of the p38MAPK/NF-κB pathway. Berberine distinctly suppressed alveolar bone loss and inflammation in rats exposed to ligature-induced periodontitis. As well as this, berberine significantly decreased the levels of phosphorylated p38MAPK and phosphorylated NF-κB 65 through upregulating the GRP30 protein levels, this protective effects of berberine were reversed by injection of G15, along with the upregulated activity of the p38MAPK/NF-κB pathway in rats with periodontitis. Berberine had a clear inhibitory effect on alveolar bone loss and inflammation in rats exposed to ligature-induced periodontitis, and its putative mechanism of action was attributed to the downregulation of the activity of the P38MAPK/NF-κB pathway, mediated by the G Protein-coupled estrogen receptor.