The Study Of Astragalus Injection On Pulmonary Fibrosis Effect In Rats Induced By Bleomycin

Objective: This study,established the Pulmonary Fibrosis model by Bleomycin-induced pulmonary fibrosis in rats,through the detection about Pulmonary Fibrosisrelated indicators, including those related to oxidative stress (SOD, MDA), smoothmuscle actin-α (α-SMA), transforming growth factor-β (TGF-β1) and its downstreamsignaling pathways TGF-β/Smads, investigates the effects of Astragalus Injection onrats Pulmonary Fibrosis model, and is to develop new drugs for the treatment ofclinical Pulmonary Fibrosis.Methods: Choose30wistar male rats and divided three groups randomly, that is,the control group (saline), the model group (BLM) and the treatment group(Astragalus Injection). The rats in the treatment group and the model group are treatedwith the method of intratracheal injection of BLM for preparing the model ofPulmonary Fibrosis. Begin to give a intraperitoneal injection on the21th days aftermodeling, the treatment group was given Astragalus Injection5ml/kg, the modelgroup was given saline5ml/kg, once a day for two weeks.1h after the lastadministration, anaesthetize the rats with10%chloral hydrate (3.0ml/kg). And thenremove the pulmonary tissue with the Abdominal aortic blood way. Centrifuge theblood samples for15mins, prepare and distribute serum. Detect the content of SODand MDA in serum, and observed the imbalance severity of oxidation and antioxidantin rats. Prepare the conventional pathological section, by HE staining, observe generalmorphology of the normal cells and diseased cells in pulmonary tissue of rats, thealveolar inflammation degree, alveolar septum and occurrence of inflammatory cellinfiltration. Observed the collagen fibers in pulmonary tissue by Masson stainingmethod, and analyze the result combined with that of the HE staining methods toidentify the degree of pulmonary fibrosis. At the same time,detect α-SMA, TGF-β1,Smad2/3expression in pulmonary tissue using Immunohistochemistry and Westernblot method. Results: From the pathological section we can observe, pulmonary tissue of themodel group has inflammatory cell infiltration and proliferation of collagen fibersobviously, while that of the treatment group improved distinctly. FromImmunohistochemistry sliced and western blot, we can observe that α-SMA, TGF-β1expression was significantly increased, TGF-β/Smads signaling pathway is activatedin the model group compared with the control group. While in the treat group, α-SMA,TGF-β1content has been effectively controlled, and inhibits TGF-β/Smads signaltransduction. By detecting the SOD activity and MDA content in serum, we observedthat serum SOD activity was significantly lower (P <0.05), and MDA levels weresignificantly increased (P <0.05) in the model group compared with the control group,and SOD was significantly higher (P <0.05), MDA decreased significantly (P <0.05)in treatment group compared with the model group.Conclusion: Astragalus injection could inhibit fibroblast transformation tomyofibroblasts by adjusting the expression of α-SMA, which play a certain inhibitionon pulmonary fibrosis. Possible mechanism of action is through inhibition of theexpression of TGF-β1Astragalus injection, and involved in the regulation of signaltransduction pathways TGF-β/Smads inhibition of pulmonary fibrosis;At the sametime Astragalus injection could enhance the vitality of SOD, reducing the level ofMDA, improving the antioxidant capacity of body, so as to achieve the purpose ofinhibiting pulmonary fibrosis.