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. 2014 Jul;5(3):172–180. doi: 10.1177/1947603514528354

Figure 1.

Figure 1.

Kartogenin blocks IL-1β-mediated loss of pericellular coat retention on articular chondrocytes as well as loss of proteoglycan retention within neocartilage. Pericellular matrices (coats) were examined on bovine articular chondrocytes cultured in monolayer. Green cells represent live cells labeled with calcein-AM (A-F) and those shown are representative of 2 independent experiments. Chondrocytes were treated with 10 ng/mL IL-1β in the presence or absence of 10 µM kartogenin for 48 hours. Kartogenin treatment alone (B) did not significantly enhance coat size seen on untreated chondrocytes (A). However, the loss of coats due to IL-1β treatment (C) was blocked by co-incubation with kartogenin and IL-1β (D). If cells were pretreated with testicular hyaluronidase for 1 hour (E), subsequent kartogenin treatment promoted the recovery of coats (F). Insets in panels A-F depict low power views of each condition. (G-J) Bovine neocartilages were treated with 10 ng/mL IL-1β in the presence or absence of 100 µM kartogenin for 48 hours. Kartogenin treatment alone (H) did not change safranin O staining, as compared with untreated neocartilages (G); however, the loss of safranin O staining induced by IL-1β treatment (I) was inhibited by co-treatment with kartogenin (J).