Glycyrrhizic acid inhibited inflammatory response in LPS-stimulated microglial BV2 cells via MAPK, Akt and NF-κB signaling pathways.

Activation of microglia plays a pivotal role in the pathogenesis of neuroinflammation-mediated neurodegenerative diseases. Glycyrrhizic acid (GA), a principal triterpenoid saponin in <i>Glycyrrhiza glabra</i>, has been reported to exhibit a range of biological activities. Nevertheless, the function of GA in microglia activation remains unclear. In this study, the effects and mechanisms of GA on the inflammatory response were investigated in the lipopolysaccharides (LPS)-stimulated microglial BV2 cells. BV2 cells were treated with GA (0, 20 and 50 μM), followed by stimulation with LPS (1 μg/mL). The results demonstrated that GA significantly inhibited the expression of tumor necrosis factor-α (TNF-α ) and interleukin-1β (IL-1β) at the mRNA and protein levels induced by LPS. Furthermore, the release of reactive oxygen species (ROS) and the migration of microglia were suppressed by GA in LPS-stimulated BV2 cells. In addition, GA reduced the activation of mitogen-activated protein kinases (MAPKs) and the phosphorylation of Akt. GA also inhibited the phosphorylation of Iκ Bα kinase (IKK) and p65, and blocked the nuclear translocation of p65 protein. The findings indicate that GA inhibited the inflammatory response in LPS-stimulated microglial BV2 cells through the suppression of MAPK, Akt, and nuclear factor-κ B (NF-κ B) signaling pathways, suggesting that GA may serve as a potential therapeutic approach for the treatment of neuroinflammation-associated neurodegenerative diseases.