Explore Yi Fei San Jie Fang Interventions Mechanism Of Pulmonary Fibrosis

Objective:This study selects Yi Fei San Jie Fang(also known as Yi Fei Zhu Yu Fang),a clinical efficacious prescription of the famous doctor of traditional Chinese medicine in yunnan province party,by drug intervention study in pulmonary fibrosis mice model,to explore the prescription interventions mechanism of pulmonary fibrosis on the party regulate PI3K/AKT/mTOR autophagy pathway,providing theoretical basis for the TCM treatment of pulmonary fibrosis.Methods:The pulmonary fibrosis model of mice was replicated by inhalation of bleomyc in.Animals were divided into blank group,model group,low does of Yi Fei San Jie Fang group,the does of Yi Fei San Jie Fang group,high does of Yi Fei San Jie Fang group,positive drug group and autophagy inhibitors + Chinese traditional medicine group,were given normal saline,Yi Fei San Jie Fang clinical equivalent dose clinic a l equivalent dose,2 times,four times the clinical equivalent dose,the pyrazole,ketone and autophagy inhibitor chloroquine jiayi lung fights to intervene,7 days,14 days,28 days 3 delivery cycle;In mice lung biopsy HE and Masson staining to observe the pathological changes,alkaline hydrolysis of hydroxyproline content in the lung tissue of mice,Western blot test LC3 B,p62,p-PI3 K,p-AKT,p-mTOR protein expression level,RT-PCR detection of TGF-?1,beclin1,COL-?,COL-? mRNA expression level relatively,preliminarily profit lung fights party through PI3K/AKT/mTO R signaling pathways regulate autophagy intervention mechanism of pulmonary fibrosis.Results:1.Pathological results of lung tissue in mice.Bronchiolar epithelium hyperplasia in the model group mice lungs,lumina l stenosis,wall thickening,inflammatory cel s infiltration,alveolar interval significa nt ly broadening,alveolar structure,trachea and around blood vessels and pulmonar y interstitial has a large number of collagen fibers deposition,pulmonary fibrosis anima l model copy success.The high and low dose of yifei powder was improved in the lung tissue pathology of mice,and the clinical equivalent dose group was improved obviously.2.Changes of hydroxyproline content in lung tissues of mice.The content of hydroxyproline in the lung tissue of the model group was increased,and the difference was significant(P<0.05).The content of hydroxyproline in the lung tissues of the mice was decreased after 7 days,14 days and 28 days,and the differe nce was statistically significant(P<0.05).3.Expression changes of TGF-?1,COL-?and COL-? were in lung tissues of mice.Lung tissue of model group mice TGF-?1,COL-?,COL-? mRNA expression level relatively increase,significant difference(P < 0.05).The relative expression levels of the mRNA in the lung tissues of the mice were decreased after 7 days,14 days and 28 days after the intervention,and the differences were statistically significant(P<0.05).4.Expression changes of LC3 B,p62,beclin1,p-PI3 K,p-AKT and p-mTOR in lung tissues of mice.The expression of LC3 B and beclin1 in the lung tissues of the model group was decreased,and the expression of p62,p-PI3 K,p-AKT and p-mTOR increased significantly(p <0.05).The expression levels of LC3 B and beclin1 in the lung tissues of mice were increased after 7 days,14 days and 28 days after the intervention,and the expression levels of p62,p-PI3 K,p-AKT and p-mTOR decreased,and the differe nce was statistically significant(p <0.05).Conclusion:1.The beneficial pulmonary asticosis can promote the decomposition and absorption of extracel ular matrix by activating the autophagy of the cel s,thereby reducing collagen deposition and thus interfering with the process of pulmonar y fibrosis disease.2.Yi Fei San Jie Fang by lowering PI3 K,AKT and mTOR phosphorylatio n levels,increase LC3 B,beclin1 autophagy marker protein expression and activation of autophagy,reduce the lung tissue hydroxyproline content and TGF-?1,COL-?,COL-? expression,occurrence and development of pulmonary fibrosis that party intervention may be one of the mechanisms.