Smad2/3 Expression Of Panax Notoginsenosides On Pulmonary Fibrosis Induced By Bleomycin In Rats

Objective:To observe Smad2/3 expression of Panax Notoginsenosides (PNS) on pulmonary fibrosis induced by bleomycin in rats and explore its mechanism.Methods:56 healthy SD rats were randomly divided into control group (CG), model group (MG), PNS group(PG)and dexamethasone group (DG). After the model of pulmonary fibrosis was established by a single intratracheal instillation of bleomycin for 24 h, the rats of PG and DG were given the drugs mentioned above, respectively, while only saline was given in MG. On day 14 and 28 after treatment,7 rats of each group were sacrificed, respectively, and the lungs were harvest for conventional pathological observation. Smad2/3 and TGF-β1 protein expression in lung tissues was detected by immunohistochemistry.Results:1.The lung tissue pathomorphology of rats in MG showed that typical pulmonary fibrosis process. Acute inflammation alteration of the lungs in MG was observed on 14th day. Collagen fibers sediments increased obviously and the structures of pulmonary alveoli were damaged on 28th day. The expression of Smad2/3 protein elevated and reached peak on 14th day, then decreased gradually and retained a high level on 28th day. The tendency of TGF-β1 protein expression was same as Smad2/3.2.After early intervention to the rats with pulmonary fibrosis, the pathomorphology of rat lungs in PG and DG showed pulmonary fibrosis variation further advanced, but the extent distinctly lower that MG. It were similar that lungs expression of Smad2/3 and TGF-β1 protein between DG, PG and MG. All those data from three treated groups are higher than CG and lower than MG (P<0.05)Conclusion:1.Smad2/3 protein showed high level expression in bleomycin-induced rats' lung tissue, which suggested that Smad2/3 protein is an important cytokine in the proceeding of pulmonary fibrosis. As a downstream signal, some functions of Smad2/3 implemented through TGF-β1 protein.2.after intervented by giving PNS, Smad2/3 expression is significantly lower than model group. PNS delay the development of pulmonary fibrosis induced by bleomycin in rats because it may inhibit expression.3.PNS had better intervention effect to pulmonary fibrosis. And compared with DEX, the side effect was mild.