Naringin Attenuates the Fibrosis of Transforming Growth Factor-Beta 1 Induced Human Embryonic Lung Fibroblasts through Nuclear Factor Kappa B Pathway

Abstract

To investigate the effect of naringin on the fibrosis of transforming growth factor-beta 1 induced human embryonic lung fibroblasts MRC-5 and its potential mechanism. MRC-5 cells were treated with different concentrations of naringin, 5 ng/ml transforming growth factor-beta 1 and 2 μmol/l nuclear factor kappa B activator phorbol myristate acetate. The experiment was divided into blank group, transforming growth factor-beta 1 group, transforming growth factor-beta 1+naringin group and transforming growth factor-beta 1+naringin+phorbol myristate acetate group. 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide, flow cytometry and scratch experiments were used to analyze cell viability, cell cycle distribution and migration ability. Western blot was used to examine protein levels. With the increase of naringin concentration, MRC-5 cell viability was gradually decreased. Compared with blank group, MRC-5 cell viability, cell cycle, migration rate, alpha-smooth muscle actin, collagen I alpha 1, fibronectin, phosphorylatednuclear factor kappa B p65 and phosphorylated-nuclear factor-kappa B inhibitor alpha expression in transforming growth factor-beta 1 group were increased. Naringin inhibited transforming growth factorbeta 1 induced MRC-5 cell proliferation, migration and fibrosis through inactivating nuclear factor kappa B pathway. Besides, nuclear factor kappa B activator phorbol myristate acetate could reverse naringinmediated the inhibition on transforming growth factor-beta 1 induced MRC-5 cell fibrosis compared with transforming growth factor-beta 1+naringin group. Naringin reduced transforming growth factor-beta 1-induced MRC-5 cell fibrosis by inhibiting nuclear factor kappa B pathway.