Effect Of Cigarette Smoke Exposure On PPAR? And Inflammatory Factors In Rat Diaphragm

Objective:Cigarette smoke exposure(CSE)is a major risk factor for chronic obstructive pulmonary disease(COPD),which can aggravate the inflammatory response in patients,interfere with protein metabolism,and induce diaphragmatic dysfunction.In order to explore the effect of CSE on PPARgamma(PPAR?)and inflammatory response in rat diaphragm tissue,this study established a corresponding model by cigarette smoke exposure,detected the changes of PPAR?,inflammatory factors and Myogenic differentiation factor(MyoD)in diaphragm tissue,and analyzed the correlation between PPAR? and inflammatory factors and Myod.Methods:Fifteen healthy male SD rats were randomly divided into cigarette smoke model group and normal control group,8 in model group and 6 in control group.The model was established by progressive CSE for 14 weeks.Rats in the control group were routinely raised without fumigation or any other intervention.The general condition and weight of rats were observed and measured during the establishment of the model.The rats in the two groups were sacrificed after 4 months,and the right middle lobe tissues and diaphragm tissues of the rats were taken.Then lung tissue and diaphragm tissue were stained with HE for pathological observation.The expression of PPAR?,tumor necrosis factor-alpha(TNF-?),interleukin-1(IL-1),IL-6,IL-8 and Myod protein in the diaphragm was detected by Western Blot and the correlation was determined.The above data were statistically analyzed using SPSS 23.0.All the counting data were expressed as mean ±standard deviation(`x±s).Two-way repeated measures analysis of variance was used to compare the body weight changes of the two groups over time.The remaining data were compared between the groups using independent sample t test.Pearson correlation analysis was used to test the correlation between PPAR? and inflammatory factors,MyoD.P < 0.05 indicated that the difference was significant.Results:1.General ConditionsRats in the model group showed slow activity,increased respiratory sounds,and decreased response,while rats in the control group did not show the above changes.The weight of rats in both groups increased with time,but the weight of rats in model group increased slowly compared with that in control group,and there was a statistical difference between two groups(P < 0.05).2.HE staining of lung tissueIn model group,alveolar structure disordered,interstitial hyperplasia and collagen fibers increased were observed,and a large number of inflammatory cells aggregated and infiltrated.In the control group,the tracheal structure of the lung tissue was intact,and the alveolar boundary was clear and the size was uniform.3.HE staining of diaphragmatic tissueIn model group,the diaphragmatic muscle tissue myofibers of rats had reduced,and disordered myocyte nuclei,enlarged myofiber intervals,increased interstitial fibers,and vascular and capillary hyperplasia were observed.In the control group,the diaphragmatic muscle myofibers were full and tightly arranged without interstitial hyperplasia.4.The content of PPAR?,inflammatory factors and MyoD protein in diaphragmThe expression of PPAR? and MyoD protein in model group rats showed a decreasing trend,and the difference was statistically significant compared with control group rats(P < 0.01).The expression of inflammatory factors IL-6 and IL-8 protein in the model group showed an upward trend,and the difference was statistically significant compared with the control group(P < 0.05).Although the expression of inflammatory factors IL-1 and TNF-? protein showed an upward trend,the difference was not statistically significant compared with the control group(P > 0.05).5.The correlation among PPAR?,inflammatory factors and MyoDThe level of PPAR? in the diaphragm of rats in the model group was significantly negatively correlated with the levels of inflammatory factors IL-6 and TNF-?(P < 0.05),while there was a significant positive correlation between PPAR? and MyoD(P < 0.05).Conclusions:CSE induced decrease in PPAR? content and significant increase in the levels of inflammatory factors IL-6 and IL-8 may be one of the mechanisms of diaphragmatic dysfunction in COPD.PPAR? may reduce MyoD content in diaphragm by regulating inflammatory response by increasing the level of inflammatory factor IL-6,thus affecting diaphragmatic function in COPD.