Effect Of Electro-acupuncture Through P38MAPK Signal Transduction Pathway In Rats With Chronic Obstructive Pulmonary Disease

BackgroundAcupuncture has a long history as a kind of treatment method,treatment of lung diseases, such as cough asthma early application, ChronicObstructive Pulmonary disease (Chronic Obstructive Pulmonary Diesase,COPD) is a limited airflow characterized by Chronic airway inflammatorydiseases. Treatment of COPD are mainly ics bronchiectasis medicine andhormone, however the two drugs were not completely improve daily life.Along with the further understanding of COPD pathogenesis, EA treatmentalso gradually applied to the treatment of COPD remission, improve thepatient’s lung function, improve the quality of life.ObjectThe research would lead to observe the electro-acupuncture for lungfunction, and various proteins regulate on the rats with chronic obstructivepulmonary disease. The early experimental results, hope to develop aneffective and safe nursing provide experimental basis for copd. At the sametime provide for the further study of the chronic obstructive pulmonarydisease. This experiment mainly research from the protein level of study, expect to provide an experimental basis for the study of protein groupfollow-up studies and signal transduction.MethodsForty male SD rats were fed for7days to adapt the environment andwere randomly divided into Control, Model, Medicationand EA fourgroups. The model of COPD was established bysmokingcombined withendotracheal injectionof lipopolysaccharide for30days.At the same timeof producing the depression model rats from the8th day,dexamethasoneacetate injection(2.0mg/kg,Intraperitoneal injection)was given to themedication group rats,once daily,continuously for22days;EA(9v,1-3mA,1.5-3Hz,D.-D.wave,)was applied to “Taiyuan”(LU9)“Zusanli”(ST36)“Fenglong”(ST40)and “Taixi”(KI3) for20min,once daily,continuously for22days. Observed under optical microscope afterhematoxylin and eosin staining (H-E staining), the expression of MMP-9and TIMP-1were assayed with immunohistochemical technique.Theexpression of phospho-p38MAPK and Ang II were assayed with westernblot method.ResultsCompared with the normal group, model group rats appeared dyspnea,cough, shortness of breath, apathetic, spit saliva, hair yellow teeth and othersymptoms and signs.H-E staining showed diffuse edema and severe inflammatory cell, thenumbers of goblet cells are increased. And more proliferation of fibroblastsin the model group compared with other three groups. The expression of phospho-p38MAPK increased significantly in lungof the model rats compared to the normal group(P<0.05); also theexpression of phospho-p38MAPK reduced significantly in lung of EA andmedication groups compared to the model group(P<0.05). There were nosignificant difference between the EA group and the medicationgroup(P>0.05).The expression of Ang II increased significantly in lung of the modelrats compared to the normal group(P<0.05); also the expression of Ang IIreduced significantly in lung of EA and medication groups compared to themodel group(P<0.05). There were no significant difference between the EAgroup and the medication group(P>0.05).The expression of MMP-9and TIMP-1increased significantly in lungtissue of the model rats compared to the control group(P<0.05); also theexpression of MMP-9and TIMP-1reduced significantly in lung tissue ofEA and medication groups compared to the model group(P<0.05). Therewere not significant difference between the EA group and the medicationgroup(P>0.05). Compared with the Control, Medication and EA group,MMP-9/TIMP-1declined in the Model group (P<0.05), and there were notsignificant difference between the EA group and the medicationgroup(P>0.05).ConclusionEA can effectively improve the lung function of COPD rats, Themechanism may be through the EA, angiotensin II, activate the p38MAPKsignaling pathway, which regulates protease-resistant protease expression.