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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: 4,8-Dicarboxyl-8,9-iridoid-1-glycoside inhibits apoptosis in human osteoarthritis chondrocytes via enhanced c-MYC-mediated cholesterol metabolism in vitro

Fig. 5

The c-MYC inhibitor 10058-F4 inhibits the proliferation of chondrocytes and promotes apoptosis and autophagy. A The c-MYC inhibitor 10058-F4 decreased the concentration of chondrocytes. B The proliferation rate of chondrocytes gradually decreased with increasing concentrations of 10058-F4. C The inhibition rate of chondrocytes gradually increased with increasing concentrations of 10058-F4. D Dose-response curve of 10058-F4 inhibition of chondrocyte proliferation. E–H 10058-F4 stimulated the proapoptotic protein caspase-3 and increased the expression of BAX, while it inhibited the expression of the antiapoptotic protein Bcl-2. However, BIG can reverse these effects caused by 10058-F4. I–K 10058-F4 promoted the expression of autophagy-related proteins Beclin-1 and LC3B. L–Q The c-MYC inhibitor 10058-F4 inhibited the chondrocyte division cycle and that BIG promoted cell division while inhibiting apoptosis. Data are presented as the mean ± SEM (n = 3) and were analysed by the Kruskal‒Wallis test. The IC50 of 10058-F4 was analysed by probit regression, *P < 0.05, **P < 0.01, ***P < 0.001

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