RESULTS: Compared with untreated mice, CS exposure caused lung functions decline manifested by increases of value on TLC, FRC, Cchord, RI and decrease FEV100/FVC. The STS intervention inhibited the lung function decline. The lung tissue sections displayed the effects of STS on inhibiting the increases on the mean linear intercept. In BAL fluid, STS relieved the increase of inflammatory cells number and of IL-6 and KC level. In lung tissue, STS abolished the downregulation of CFTR caused by cigarette smoke exposure. In 16HBE cells, STS inhibited CFTR decrease, ERK1/2 phosphorylation, Nrf2 upregulation and nuclear translocation, and IL-6 and IL-8 secretion induced by CSE. However, STS could not reverse the enhancing effects of inh-172 pretreatment on ERK1/2 phosphorylation, Nrf2 nuclear translocation and IL-6 secretion induced by CSE.