Geniposide Suppresses Interleukin-1β-Induced Inflammation and Apoptosis in Rat Chondrocytes via the PI3K/Akt/NF-κB Signaling Pathway

Abstract

Osteoarthritis (OA) is a chronic degenerative joint disease that is principally characterized by progressive joint dysfunction and cartilage degradation. Inflammation and apoptosis play critical roles in the progression of OA. Geniposide (GPO), one of the principal components of the fruit of Gardenia jasminoides Ellis, has been reported to have anti-inflammatory and other pharmacological effects. In this study, we performed in vitro experiments on rat chondrocytes to examine the therapeutic effects of GPO on OA and investigated its effects in vivo in a rat model of OA induced by medial meniscal tear (MMT). The results suggest that GPO can inhibit the expression of INOS, COX-2, and MMP-13 in vitro, and promote the expression of collagen II in rat chondrocytes stimulated with interleukin-1β (IL-1β). In addition, we also found that GPO can inhibit the expression of pro-apoptotic proteins such as Bax, Cyto-c, and C-caspase3 and increase the expression of the anti-apoptotic protein Bcl-2. These changes may be related to GPO-induced inhibition of the IL-1β-induced activation of the PI3K/Akt/NF-κB signaling pathway. In vivo, we also found that GPO can limit the development of OA in a rat model. Taken together, the above results indicate that GPO has potential therapeutic value for treating OA.

Keywords: PI3K/Akt/NF-κB; apoptosis; chondrocyte; geniposide; inflammation; osteoarthritis.