| Objective Diseases of the respiratory system have multiple manifestations,which may be manifested as impaired respiratory function but also involve other systems of the whole body.Chronic obstructive pulmonary disease is a typical respiratory disease.Although it has been studied throughout the history of respiratory disease research,its mechanism is not fully understood.Studies have shown that the main mechanisms involved in the pathogenesis of COPD include inflammation,oxidative stress,genetic factors,pulmonary microbial variation,and autoimmunity.Peroxisome proliferator activated receptorγ（PPARγ）is a ligand-dependent nuclear receptor that is highly expressed in human and rodent lungs.15-Deoxy-delta-12,14-prostaglandin J2（15d-PGJ2）,cyclopentanone prostaglandin,is an endogenous ligand of PPARγ.Studies have confirmed that PPARγand 15d-PGJ2 play a crucial role in the process of oxidative stress.However,the association between PPARγ,15d-PGJ2 and chronic obstructive pulmonary disease（COPD）remains unclear.In this study,based on the available basic data of COPD patients,serum and lung tissue,the relationship between serum 15d-PGJ2 and lung function,PPARγexpression in lung tissue and oxidative stress markers in tissues was investigated through a case-control study.Furthermore,the correlation of 15d-PGJ2 on oxidative stress level and PPARγexpression in TNF-α-induced BEAS-2B cells was verified by in vitro cell experiments.Methods A total of 130 COPD patients admitted to the respiratory Department of the Second Affiliated Hospital of Anhui Medical University were selected,and an equal number of healthy volunteers without pulmonary disease were selected from the physical examination center.Clinical information of the two groups was collected.The serum levels of 15d-PGJ2 were detected by ELISA.At the same time,40 COPD patients and normal lung tissues were collected from the thoracic surgery Department of the Second Affiliated Hospital of Anhui Medical University,and PPARγexpression was detected by immunohistochemical method.The expression levels of oxidative stress markers（NOX-4 and HO-1）in lung tissues were detected by Western blotting.The cells were pretreated with 0.1mmol/m L 15d-PGJ2 for 24h,then 20 ng/m L TNF-αwas added for 24h,and the cells were collected.The expression of PPARγin the cells was detected by immunofluorescence method,and the total protein was extracted.Western blotting detected the levels of markers of oxidative stress in the cells.Results Serum 15d-PGJ2 was reduced in COPD patients compared with healthy volunteers.Linear and logistic regression analysis indicated that serum 15d-PGJ2 was positively associated with pulmonary function in COPD patients.Additionally,PPARγ-positive nuclei were reduced and oxidative stress indicators,included HO-1and NOX-4,were increased in lungs of COPD patients.Further correlative analysis suggested that pulmonary function parameters was positively correlated with serum15d-PGJ2 and pulmonary PPARγ-positive nuclei,inversely related with oxidative stress indicators in lungs of COPD patients.Pretreatment with 15d-PGJ2 obviously attenuated TNFα-induced oxidative stress in BEAS-2B cells.Conclusion Serum 15d-PGJ2 and pulmonary PPARγdecreased and oxidative stress levels increased in COPD patients.Moreover,with the higher grade of COPD patients,the lower level of 15d-PGJ2 was more obvious.15d-PGJ2 was positively correlated with lung function,and serum 15d-PGJ2 was negatively correlated with oxidative stress in COPD patients.Downregulation of PPARγmay be involved in the process of oxidative stress and COPD induced by low 15d-PGJ2... |
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