Effects of Cyclopamine on the Viability of Articular Chondro | 47366

Journal of Arthritis

ISSN - 2167-7921


Effects of Cyclopamine on the Viability of Articular Chondrocytes in Rats with Adjuvant Arthritis In Vitro and Part Mechanisms

Xianbing Song, Bao Zhang, Wang Taorong, Gaoyuan Wang, Yanping Huang, Ye Zhang, Meimei Liu and Xiaoyu Chen

The aim of the present study was to investigate the effect of cyclopamine, a hedgehog signaling pathway inhibitor, on Adjuvant Arthritis (AA), rat articular chondrocyte viability and part mechanisms in vitro. In this study, an AA rat model was established by Freund’s Complete Adjuvant (FCA), and the Arthritis Index (AI), secondary paw swelling degree and HE staining was used to evaluate whether the model was successfully established. Chondrocytes of the ankle joint of AA rats were cultured and identified. Cyclopamine (0, 0.03, 0.1, 0.3, 1, 3, 10 and 30 mg/L) was administered to determine chondrocyte viability. Chondrocyte apoptosis was detected by Annexin V-FITC/PI double dye. The expression of hedgehog signaling pathway-related proteins Shh, Ptch1 and Gli1 in chondrocytes was detected by western blotting. The results showed that AA was successfully induced by FCA, since the AI of AA rats and secondary paw swelling degree increased, the cartilage tissue of the rats’ ankle joint was damaged, and the chondrocytes were successfully cultured in vitro following the identification of toluidine blue and type II collagen. Cyclopamine (0.03, 0.1, 0.3, 1, 3, 10 and 30 mg/L) could increase the viability of chondrocytes in vitro and reduce the apoptotic rate of chondrocytes. As compared with the control group, different doses of cyclopamine (0.3, 3 and 10 mg/L) significantly decreased the expression of Shh, Ptch1 and Gli1 proteins in AA chondrocytes. Therefore, in the present study, an AA rat model was successfully established, and cyclopamine inhibited the viability and apoptosis of chondrocytes, an effect that may be associated with the inhibition of the chondrocyte hedgehog signaling pathway.