Study On The Mechanism Of Yifei Sanjie Method Regulating COPD Airway Remodeling Based On NF-kappa B And TGF-beta1/Smads Signal Pathway

Objective:Based on COPD airway remodeling "Qi deficiency,blood stasis and phlegm obstruction" in TCM Pathogenesis,this research selects the Yunnan Province Famous Traditional Chinese medicine Professor Li Qingsheng's clinical empirical prescription in treating COPD-Yuping wind powder modified prescription and its "cleanse phlegm" and the "expel blood stasis" drug group,to discuss the mechanism of the effect of this recipe and its drug group on alleviating airway inflammation and intervening in airway remodeling development,and to elucidate the mechanism of the effect of Yifei Sanjie method on regulating COPD airway remodeling,providing experimental basis and theoretical reference for Chinese medicine treating COPD.Method:The COPD airway remodeling model was replicated in rats by smoking and intratracheal injection of LPS.Yuping wind powder modified prescription and its "cleanse phlegm" and the "expel blood stasis" drug group were given intervention.Morphological changes of lung tissue were observed by HE staining.The levels of NF kappa B,Smad2/3 and Smad7 were detected by immunohistochemistry and Western-blot in rats.MRNA relative expression levels of TGF-beta 1 in rat lung tissues were detected by RT-PCR.The levels of cytokines in rats at different administration periods were observed.Result:1.Pathological findings of HE staining in lung tissue of rats Chinese medicine intervention group compared with the model group,rat pulmonary septum,bronchiolar epithelial hyperplasia,necrosis,shedding,stenosis,wall thickening,fibrous tissue hyperplasia,inflammatory cell infiltration,pulmonary bulla and other pathological changes were alleviated,in the 4 weeks after the model of drug delivery phase,the high dose group of Yupingfengsan flavored was the most obvious.2.Changes of NF kappa B,TGF-beta 1's m RNA,Smad2/3 and Smad7 expression in lung tissue of rats NF-kappa B,Smad2/3,Smad7 mainly expressed in the bronchial wall and surrounding inflammatory cells in cytoplasm.The positive expression of NF-kappa B and Smad2/3 was increased in model group,and the positive expression of Smad7 was decreased.In the drug intervention group,the positive expression of NF-kappa B and Smad2/3 was decreased,and the positive expression of Smad7 was increased.In the prevention of drug delivery phase,the drug delivery after the mode set up phase and the 4 weeks after the model of drug delivery phase,the m RNA relative expression levels of TGF-beta 1 in the model group were up regulated,the expression level of Smad7 in the model group decreased in the 8 weeks after the model of drug delivery phase,the difference was significant(P < 0.05).Compared with the model group,the TGF-?1m RNA expression level of Yupingfengsan flavored high and middle dose group and Ditan middle dose group in the drug delivery after the model set up phase,Yupingfengsan flavored group and Ditan group and Zhuyu middle and low group in the 4 weeks after the model of drug delivery phase were down-regulated,the Smad7 expression level of Yupingfengsan flavored high group and Ditan high and middle group and Zhuyu high and middle group in the 8 weeks after the model of drug delivery phase were up-regulated,the difference was significant(P < 0.05).Yupingfengsan flavored high group in the drug delivery after the model set up phase decreased NF-kappa B expression significantly,Ditan middle group in the 8 weeks after the model of drug delivery phase decreased NF-kappa B significantly(P < 0.05).In the high and middle dose groups,TGF-?1m RNA in the drug delivery after the model set up phase was decreased,which was significant in the Yupingfengsan flavored group,in the intervention group,TGF-?1m RNA in the 8 weeks after the model of drug delivery phase was decreased significantly(P < 0.05).Zhuyu high and middle groupin the 8 weeks after the model of drug delivery phase decreased Smad2/3 expression significantly(P < 0.05).Conclusion:1.It is one of the mechanisms that regulate the airway remodeling of COPD by regulating the NF-kappa B and the TGF-beta 1/Smads signaling pathway by supplementing qi and eliminating phlegm and blood stasis.2.Yupingfengsan flavored and "phlegm" and "blood stasis" drug group can reduce the lung tissue NF-kappa B expression,inhibite the NF-kappa B signaling pathway activity,alleviate airway inflammation;through the down-regulation of TGF-beta 1,reduce the expression levels of Smad2/3,up-regulate the expression levels of Smad7,intervent airway remodeling.