Skip to main content
Fig. 4 | Arthritis Research & Therapy

Fig. 4

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. 4

BIG upregulates the expression of cell cycle-related proteins to inhibit apoptosis and autophagy in chondrocytes in OA. A BIG promoted the upregulated expression of cyclin CCNH. B, E, F BIG promoted the upregulation of proteins associated with degradation in OA chondrocytes. C BIG promoted the upregulation of chondrogenesis-related proteins. D BIG effectively caused high expression of the pro-cell division protein MYC. G Immunofluorescence confocal images show a peak in cytoskeletal protein α-tubulin replication on day 9 of chondrocyte coculture with BIG (× 400). H, J–L BIG effectively inhibited the expression of BAX, cleaved caspase-3, and Beclin-1. I BIG caused a gradual decrease in the autophagy ratio in OA chondrocytes, and the autophagy ratio decreased significantly in the BIG group than in the cell group. O–S BIG significantly increased Bcl-2 expression but decreased the expression of BAX, cleaved caspase-3, caspase-3, Beclin-1, and LC3B. Data are presented as the mean ± SEM (n = 3) and were analysed by the Kruskal‒Wallis test, *P < 0.05, **P < 0.01, ***P < 0.001

Back to article page