Thalidomide inhibits the gene promoter of connective tissue growth factor in human embryonic lung fibroblasts

Background: The etiology and pathogenesis of idiopathic pulmonary fibrosis (IPF) remain unclear, and the early detection and treatment are vital to the prognosis of IPF patients. It's necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-I beta (TGF-beta 1) in human embryonic lung fibroblast (HELF). Methods: The gene vector of pGL3-CTGIT containing human CTGF gene promoter was constructed and transfected into HELF cells. We used different TGF-beta 1 (0, 2.5, 5, 10 and 20 mu g/L respectively) to stimulate HELF to identify the optimal concentration for gene promoter of CTGE The activity of luciferase was measured to observe the effect of TGF-beta 1 and THALIDOMIDE on the activity of CTGF gene promoter. Results: The relative luciferase activity increased significantly with the stimulation of TGF-131, and the relative luciferase activity peaked in the 5 mu g/L TGF-beta 1 group (all P<0.01). The thalidomide inhibited the TGF-beta 1-induced activation of CTGF gene promoter in HELF, and the effect peaked in the 25 mu g/L group (all P<0.001). Conclusions: Thalidomide produces a significant inhibitory effect on the gene promoter activation of CTGF induced by TGF-beta 1 in I I ELF, it may be a potentially effective drug for the treatment of pulmonary fibrosis.