Effects Of Erythromycin On Expression Of Smad3and Smad7in Human Fetal Lung Fibroblast Induced By Transforming Growth Factor-β1

Objectives: The present study investigated the effects of erythromycin onexpression of smad3smad7in human fetal lung fibroblast(MRC-5) induced bytransforming growth factor-β1, and toexplore whether inhibited MRC-5proliferationand collagen production and discussed possible mechanism, seek effective medicinefor pulmonary fibrosis, which can provides experimental foundation for clinictherapy.Methods: In vitro MRC-5cultured to the exponential growth phase withdifferent concentration of erythromycin, then treated with TGF-β1, the role of acertain time, choose a proper concentration of erythromycin for treating MRC-5through the cells inhibition and proliferation by MTT assay. Thereafter,The MRC-5were divided into four groups: group1(control), cells cultured with MEM/NEAA;TGF-β1group, cells cultured with TGF-β1(5μg/ml); TGF-β1+EM pre-treatment group,cells were treat with a proper concentration of EM for12hours, then plusedTGF-β1(5μg/ml) for24hours, TGF-β1+EM post-treatment group cells were culturedon the opposite way. All of the group, MTT method and hyp alkaline hydrolysis wereapplied to evaluate the fibroblasts proliferation and collagen production respectively,the expression of mRNA of Smad3and Smad7by RT-PCR and for expression ofp-Smad3、Smad3and Smad7protein assay by western blotting.Results: Compare with TGF-β1group, EM group decreased fibroblastproliferation and the collagen production is lower. The difference was significant ofstatistics(P<0.05). Among of then, T+Pre-EM is the Lower in MRC-5. the expressionof Smad3mRNA and p-Smad3protein is lower than TGF-β1group, The decline ofT+Pre-EM is the most. Smad7mRNA and protein were higher than TGF-β1group.However, T+Pre-EM is the highest. Conclusions: Erythromycin could inhibit the MRC-5’s proliferation and collagenproduction which induced by transforming growth factor-β1. It may have importantrole in the delaying lung fibrosis forming progress. Its mechanism may be influce thesignaling mediated by smad.