Figure 5.

GTX influences osteoblast differentiation via the inhibition of NF-κB signaling in C2C12 cells. (A) Western blot analysis and (B) immunofluorescence confocal microscopic assay revealed that treatment with 10 ng/ml TNF-α induced the aggregation of NF-κB protein p65 in the nucleus; however, this effect was abrogated following 1 μg/ml GTX treatment. (C) Luciferase assay indicated that the activation of NF-κB transcriptional activity induced by BMP-2 + TNF-α treatment was abrogated by GTX treatment in a dose-dependent manner. ^*P<0.05, ^**P<0.01, n>3. GTX, gliotoxin; NF-κB, nuclear factor-κB; TNF-α, tumor necrosis factor-α; BMP-2, bone morphogenetic factor-2; NC, normal control.