| ObjectiveChronic obstructive pulmonary disease(COPD)is a kind of chronic disease which seriously affects our national health and causes diaphragm dysfunction.Systemic inflammation is a major risk factor for diaphragm dysfunction in COPD.Wnt/β-catenin/PPARγ is involved in chronic inflammation of COPD.Aerobic exercise is a common rehabilitation method in COPD lung rehabilitation,and aerobic exercise has been reported to improve systemic inflammation of COPD,but the specific mechanism is still unclear.Therefore,this study is to investigate the effects of aerobic exercise on the inflammation of diaphragm tissue and Wnt/β-catenin/PPAR γ in rats with COPD.MethodTwenty-four healthy male SD rats were randomly divided into blank control group,model control group and aerobic exercise group,with 8 rats in each group.Rats in the model control group and the aerobic exercise group were established as COPD models through 16 weeks of incremental cigarette smoke exposure.Rats in the blank control group were routinely fed without fumigation or any other intervention.The model was judged after the modeling was finished.After the modeling,the aerobics group underwent a nine-week intervention of moderate intensity swimming in a water tank.Model control group did not receive any intervention.After the exercise intervention,the rats were subjected to intraperitoneal anesthesia,and lung tissues and diaphragmatic tissues were collected.The pathological changes of lung tissue and diaphragm tissue were observed by HE staining.The protein expressions of Wnt1,β-catenin,PPARγ,IL-1β,IL-6,IL-8 and TNF-α in the diaphragm tissue of rats were quantitatively detected by Western blot.Results(1)HE staining of lung tissueIn the model control group,the alveolar structure was disordered,interstitial hyperplasia,collagen fibers increased,and a large number of inflammatory cells accumulated and infiltrated In aerobic exercise group,the airway mucosa hyperplasia was reduced,the airway wall became thinner,the inflammation infiltration was reduced,and the damage of alveolar structure was improved.(2)HE staining of diaphragm tissueIn the blank control group,the muscle fibers of the diaphragm were full,closely arranged and without interstitial hyperplasia;in the model control group,the muscle fibers of the diaphragm tissue were reduced,the nuclei of the muscle cells were disordered,and the muscle fiber septum was enlarged,there were more interstitial fibers and proliferation of blood vessels and capillary,and in the aerobic exercise group,the arrangement and shape of the diaphragm fibers were more regular,the muscle fiber gap was slightly widened,and the muscle fiber breakage and atrophy were alleviated than those in the control group.(3)The content of Wnt1,β-catenin and PPARγ protein in diaphragmCompared with the blank control group,the expression levels of β-catenin and PPARγ protein in the diaphragm tissue of model control group were significantly decreased(P<0.05,P<0.01),and Wnt1 had a decreasing trend;Compared with model control group,the protein expression levels of Wnt1,β-catenin and PPARγ in diaphragm tissue of rats in aerobic exercise group were significantly increased(P<0.05,P<0.01).(4)The content of IL-1β,TNF-α,IL-6 and IL-8 protein in diaphragmCompared with blank control group,the protein expression levels of IL-1β,IL-6and IL-8 in diaphragm tissue of model control group were significantly increased(P<0.05,P<0.01),and TNF-α had an increasing trend;Compared with model control group,the protein expression levels of IL-1β and IL-8 in diaphragm tissue of rats in aerobic exercise group were significantly decreased(P<0.05,P<0.01);The protein expression levels of TNF-α and IL-6 decreased.Conclusions(1)Cigarette smoke exposure resulted in decreased expression of Wnt1,β-catenin,PPARγ and inflammatory cytokine ILThe expression of 1β,IL-6,IL-8 and TNF-α increased,which may be one of the mechanisms of diaphragmatic dysfunction in COPD.(2)Cigarettes smoke exposure induced pathological damage of lung tissue and diaphragm tissue in COPD rats;Aerobic exercise can slow down the pathological damage process of lung tissue and diaphragm tissue in COPD rats,which is beneficial to delay the development of the disease.(3)Aerobic exercise can significantly improve diaphragmatic inflammation in COPD rats,and the mechanism of action may be related to the inflammatory signaling pathway involved in Wnt/β-catenin/PPARγ. |
