Galangin inhibits lipopolysaccharide-induced inflammation and stimulates osteogenic differentiation of bone marrow mesenchymal stem cells via regulation of AKT/mTOR signaling

Background: Bone marrow mesenchymal stem cells (BMSCs), with the abilities of multidirec-tional differentiation and self-renewal, have been widely used in bone repair and regeneration of inflammation-stimulated oral diseases. Galangin is a flavonoid isolated from Alpinia officinarum, exerts anti-obesity, antitumor, and anti-inflammation pharmacological effects. The roles of galangin in lipopolysaccharide-induced inflammation and osteogenic differentiation of BMSCs were investigated. Methods: BMSCs were isolated from rat bone marrow and identified by flow cytometry. The isolated BMSCs were treated with 1 μg/mL lipopolysaccharides or cotreated with lipopolysaccharides and different concentrations of galangin. Cell viability and apoptosis were detected by MTT (tetrazolium component) and flow cytometry. ELISA was used to detect inflammation. Alizarin red staining was used to investigate osteogenic differentiation. Results: The rat BMSCs showed negative rate of CD34, and positive rate of CD29 and CD44. Lipopolysaccharides treatment reduced cell viability of BMSCs, and promoted the cell apoptosis. Incubation with galangin enhanced cell viability of lipopolysaccharide-stimulated BMSCs, and suppressed the cell apoptosis. Galangin decreased levels of TNF-α, IL-1β, and IL-6 in lipo-polysaccharide-stimulated BMSCs through down-regulation of NF-κB phosphorylation (p-NF-κB). Galangin up-regulated expression of osteo-specific proteins, collagen type I alpha 1 (COL1A1), osteopontin (OPN), and runt-related transcription factor 2 (RUNX2), to promote the osteogenic differentiation of lipopolysaccharide-stimulated BMSCs. Protein expression of p-AKT and p-mTOR in lipopolysaccharide-stimulated BMSCs were increased by galangin treatment.  Galangin exerted an anti-inflammatory effect against lipopolysaccharide-stimulated BMSCs and promoted osteogenic differentiation through the activation of AKT/ mTOR signaling.