Astilbin-induced inhibition of the PI3K/AKT signaling pathway decelerates the progression of osteoarthritis

Degeneration and destruction of articular cartilage are the key characteristics of osteoarthritis (OA). In recent studies, the use of astilbin (AST), the primary active ingredient of Astilbe chinensis, has been shown to correlate with a reduction in inflammatory disease symptoms. The present study aimed to investigate the effects and mechanisms of AST on OA. A rat model of OA was constructed and in vivo experiments were performed using the AST, PBS, OA and control groups. The cartilage tissues of each group were assessed by hematoxylin and eosin and toluidine blue staining. The gene expression levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, AKT, PI3K and other related proteins were analyzed by reverse transcription-quantitative PCR and western blot analysis. AST was found to significantly inhibit IL-1β and TNF-α protein expression; this further confirmed that IL-1β, TNF-α and PI3K mRNA expression was downregulated, indicating that the protective mechanism of AST is associated with the PI3K/AKT pathway. Overall, the results of the present study demonstrate that AST can improve OA symptoms by downregulating the PI3K/AKT signaling pathway, and may therefore be a potential therapeutic option for patients with OA.

Keywords: PI3K/AKT signaling pathway; astilbin; inflammatory cytokines; osteoarthritis.