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. Author manuscript; available in PMC: 2013 May 1.

Published in final edited form as: Clin Immunol. 2012 Feb 10;143(2):188–199. doi: 10.1016/j.clim.2012.01.019

Inhibition of LPS-stimulated IL-6 secretion from fibroblasts by knocking down NFκB p65 or pharmacological inhibitor. A. Gingival fibroblasts were transfected with p65 siRNA or control siRNA for 48 h and then treated with or without 100 ng/ml of LPS for 24 h. After the treatment, p65 and IL-6 mRNA were quantified using real-time PCR and normalized to GAPDH mRNA. B. Inhibition of LPS-stimulated IL-6 secretion from gingival fibroblasts by NFκB inhibitor parthenolide. Gingival fibroblasts were treated with 100 ng/ml of LPS in the absence or presence of different concentrations of parthenolide as indicated for 24 h. After the treatment, IL-6 in culture medium was quantified using ELISA. The data (mean ± SD) presented are representative of two independent experiments with similar results.

Inhibition of LPS-stimulated IL-6 secretion from fibroblasts by knocking down NFκB p65 or pharmacological inhibitor. A. Gingival fibroblasts were transfected with p65 siRNA or control siRNA for 48 h and then treated with or without 100 ng/ml of LPS for 24 h. After the treatment, p65 and IL-6 mRNA were quantified using real-time PCR and normalized to GAPDH mRNA. B. Inhibition of LPS-stimulated IL-6 secretion from gingival fibroblasts by NFκB inhibitor parthenolide. Gingival fibroblasts were treated with 100 ng/ml of LPS in the absence or presence of different concentrations of parthenolide as indicated for 24 h. After the treatment, IL-6 in culture medium was quantified using ELISA. The data (mean ± SD) presented are representative of two independent experiments with similar results.