Mechanism of Baicalein in the treatment of arthritis by regulating JNK/ERK/p38MAPK and PI3K/Akt signaling pathways

Abstract The present study aimed to investigate the anti-inflammatory effects of Baicalein on human osteoarthritic chondrocytes and its molecular mechanisms, and to explore the related molecular events that may occur. The extracted human osteoarthritic chondrocytes were stimulated with interleukins. After administered with different concentrations of Baicalein, the survival rate of chondrocytes was observed. Apoptosis was detected by apoptosis assay kit. The effect on NO production was detected using the Griess reagent kit. The expressions of IL-6 and PGE2 were detected by ELISA. The apoptotic proteins and PI3/Akt, NF-kB and MAPK cascade proteins were detected by WB assay. Baicalein significantly increased the survival rate of chondrocytes and decreased the expressions of NO, IL-6 and PGE2. The expressions of COX-2 and induced iNOS were significantly reduced in a dose-dependent manner under the administration of Baicalein. In addition, Baicalein significantly reduced the NF-κB signaling pathway, inhibited the activation of the induced PI3/Akt, JNK, ERK and p38 MAPK cascades. Inflammatory mediators play a key role in the pathogenesis of osteoarthritis. Baicalin significantly inhibits the expression of inflammatory mediators in chondrocytes of human osteoarthritis and regulates the JNK/ERK/p38 MAPK and PBK/Akt signaling cascades. The experiment evaluated the anti-inflammatory and anti-osteomyelitis effects of Baicalein in order to discover new treatment strategies.