Diallyl sulfide attenuates transforming growth factor-β-stimulated pulmonary fibrosis through Nrf2 activation in lung MRC-5 fibroblast

- Diallyl sulfide (DAS) induces HO-1 expression in human lung MRC-5 fibroblast.
- DAS reduces collagen 1 mRNA level in TGF-β-induced fibrosis in MRC-5 cells.
- Suppression of Smads pathway was caused by DAS after TGF-β exposure.
- Treatment with DAS inhibits pulmonary fibrosis-related biomarkers.
- DAS has a potential effect on improving pulmonary fibrosis.

Idiopathic pulmonary fibrosis accounts for the lethal diffuse fibrosing lung disease, which is described with accumulation of fibroblasts, the loss and damage of lung epithelial cells, and causing respiratory failure. Excessive ROS level impairs the cellular redox level, inflammatory cell infiltration and abnormal collagen production to induce extracellular matrix accumulation. Nuclear factor-erythroid 2 related factor 2 (Nrf2) regulates antioxidant-associated genes as phytochemical target in chemoprevention. The preventive effect of organosulfuric compound diallyl sulfide (DAS) on TGF-β-induced fibrosis in lung MRC-5 fibroblast was investigated in this study. MRC-5 cells were pretreatment with DAS before 10 ng/mL TGF-β stimulation. DAS suppressed the collagen production in TGF-β-induced cells by attenuating Smad 2/3 phosphorylation through activating HO-1 level. DAS inhibited TGF-β-induced myofibroblast formation by decreasing ROS through enhancing Nrf2-related antioxidant enzyme and myofibroblast apoptosis. DAS is a potential dietary agent to inhibit TGF-β-induced fibrosis and to prevent oxidative stress-induced pulmonary fibrosis.