Anti-inflammatory and anti-osteoarthritis effects of tectorigenin

Abstract

Osteoarthritis (OA) is a common and dynamic joint disease, including the articular cartilage, underlying bones, and synovium. In particular, OA is considered as the degeneration of the cartilage. Tectorigenin (Tec) can affect many biological processes. However, its effect on articular chondrocytes remains unclear. This study aimed to assess the role of Tec in articular cartilage. In vitro, Tec inhibited the expression levels of type X collagen, cyclooxigenase-2, matrix metalloproteinase (MMP)-3, and MMP-13 gene but enhanced those of Runx1, type II collagen, and aggrecan in the presence of IL-1β. Meanwhile, Tec inhibited apoptosis through the Bax/Bcl-2/caspase-3 pathway, upregulating p-Bad, downregulating Bax/Bcl-2 ratio, and activating caspase-3 compared with IL-1β treatment only. Moreover, this process was partially regulated by NF-κB P65. In vivo, the chondroprotective effect of Tec was assessed by establishing a model of surgically induced OA. Tec-treated joints exhibited fewer osteoarthritic changes than saline-treated joints. Meanwhile, 1.5 µg/kg Tec treatment produced better protective effect than 0.75 µg/kg. Osteoarthritis Research Society International scoring system were employed to assess histopathological grading of the models , as well as the outcomes of immunohistochemistry for Aggrecan Neoepitope and MMP-3, further confirmed the results. In conclusion, this study showed that Tec played a chondroprotective role on the OA process by preventing articular cartilage degeneration and chondrocyte apoptosis via the NF-κB P65 pathway.