Articular cartilage degradation is prevented by tanshinone IIA through inhibiting apoptosis and the expression of inflammatory cytokines.

Abstract

The present study aimed to investigate the effect of tanshinone IIA on the degradation of articular cartilage in a rat model of osteoarthritis (OA). The OA rat model was established by anterior cruciate ligament transection (ACLT) and medial meniscus resection (MMx). The animals were treated for 28days with 0.25‑0.5mg/kg doses of tanshinoneIIA following ACLT+MMx. The knee joints of the rats in the ACLT+MMx group exhibited marked alterations in articular cartilage histopathology and higher Mankin scores, compared with those in the normal group. TanshinoneIIA treatment at a dose of 0.5mg/kg significantly inhibited cartilage degradation and improved Mankin scores in the OA rat model (P<0.002). TanshinoneIIA treatment completely inhibited the ACLT+MMx‑induced accumulation of inflammatory cells and disintegration of synovial lining in the rats. An increase in the dose of tanshinoneIIA between 0.25 and 0.5mg/kg reduced the proportion of apoptotic chrondrocytes from 41 to 2% on day 29. Treatment of the rats in the ACLT+MMx group with 0.5mg/kg doses of tanshinoneIIA markedly inhibited the expression level of matrix metalloproteinase and increased the expression of tissue inhibitor of metalloproteinase in the rat articular cartilage tissues. TanshinoneIIA treatment significantly reduced the levels of inflammatory cytokines, including interleukin‑1β, tumor necrosis factor‑α and nitric oxide in rat serum samples. The protein expression levels of bone morphogenetic protein and transforming growth factor‑β were significantly increased by tanshinone IIA in the ACLT+MMx rats. Therefore, tanshinone IIA inhibited articular cartilage degradation through inhibition of apoptosis and expression levels of inflammatory cytokines, offering potential for use in the treatment of OA.