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. Author manuscript; available in PMC: 2020 Nov 30.
Published in final edited form as: Biochem Pharmacol. 2019 Mar 9;165:79–90. doi: 10.1016/j.bcp.2019.03.014

Fig. 1. Erythromycin (EM) inhibits the catabolic activity of IL-1β on primary human articular chondrocytes (nHACs).

Fig. 1.

(A) Live-dead assay on chondrocytes treated with EM (1, 10 and 100μM) for 4 days. Percentage of dead cells/total cells was quantified. (B) RT-qPCR analysis of Col-II, Col-X, iNOS, MMP1, MMP9 and MMP13 on nHACs treated with EM (0, 1, and 10μM) and IL-1β (1ng/mL). TBP served as a reference gene for normalization. (C) NF-κB transactivation assay. nHACs were transiently transfected with an NF-κB reporter and treated with EM (10μM) and IL-1β (1ng/ml). A Renilla luciferase construct was co-transfected as an internal control for normalization. Data were reported as mean ± SD and analyzed by Dunnett’s test (B) and an unpaired t-test (C). At least three independent experiments were performed. * p<0.05.