Effect Of Hydrogen Therapy On The Expression Of SOD,MDA,PINK1 And Parkin In Lung Tissue Of COPD Rats

Objective:Through research the effects of hydrogen in pathology to a cigarette-smoke induced chronic obstructive pulmonary disease rat model,observe the expression of the related indicators of oxidation and antioxidation?SOD,MDA?and mitochondrial autophagy?PINK1,Parkin?in COPD rat lung tissue,to discuss the effects of hydrogen in delaying the development of COPD and its mechanisms.Methods:1 70 healthy male Sprague-Dawley rats?body weight 160-200 g?were randomized into the following seven groups?10 rats in each group?:control group,COPD group,low-hydrogen group?Hl group?,intermediate Hydrogen group?Hm group?,high-Hydrogen group?Hh group?,very high Hydrogen?Hvh group?,and oxygen group?O₂ group?.The rats with COPD-like lung disease were established by the smoking method.The daily condition of rats were observed.2 Xanthine oxidase method was used to measure the level of SOD in lung homogenate of rats in each group,and thiobarbituric acid colorimetric assay was used to measure the level of MDA in lung tissue of each group.Hematoxylin and eosin?HE?staining was used to observe the pathological changes of lung tissue in each group.Immunohistochemistry and WB technique were used to detect the expression of PINK1 and Parkin in lung tissue.Results:1 Comparison of SOD and MDA in lung homogenate of each groupSOD activity:Compared with the control group,the COPD group decreased significantly?P<0.01?;compared with the COPD group,Hvh,Hh group was significantly increased?P<0.01?,Hm,Hl,O₂ group was increased?P<0.05?;Hvh group significantly higher than Hh,Hm,Hl,O₂ group?P<0.01?.MDA content:Compared with the control group,the COPD group was significantly increased?P<0.01?;compared with the COPD group,Hvh,Hh group was significantly decreased?P<0.01?,Hm,Hl group was decreased?P<0.05?.2 pathologic changes of lung in cigarette smoke-induced rat modelIn the control group,the ciliated columnar epithelium of the tracheal mucosa was intact in the rat lung tissue.There was no inflammatory cell infiltration around the airways,no expansion and congestion of the capillaries,and normal alveolar size and structure.Compared with the control group,the lung volume in the COPD group was increased;on gross morphology,it was white and uneven,rather than smooth,and had poor flexibility.Under the microscope,the alveolar ducts,alveolar sacs and pulmonary alveoli were significantly expanded,the alveoli were structurally disordered,the alveolar wall showed signs of thinning and breaking,and some had fused into bullae,the ciliated cells degenerated and necrosis,the pulmonary arterial wall thickened,the lumen narrowed,and a large number of inflammatory cell infiltrates around.The volume of lungs in Hvh,Hl,Hm,Hh and O₂ groups was slightly smaller than that in COPD group,and the appearance was also improved.Pulmonary arterial wall thickening is more limited,with varying degrees of inflammatory cell infiltration,but compared with the COPD group to varying degrees of reduction.The alveolar walls were thin,with varying degrees of fracture,but improved compared with the COPD group3 Protein of PINK1 and Parkin of the lung tissue was detected by immunohistochemistry.Compared with control group,Parkin protein expression in COPD group increased.Compared with COPD group,the expression of Parkin protein in Hvh,Hh,Hm,Hl group decreased,but there was no significant difference in O₂ group.There was no significant difference in the expression of PINK1protein among the groups.4 Protein of PINK1 and Parkin of the lung tissue was detected by Western blot.Compared with control group,Parkin protein expression in COPD group increased.Compared with COPD group,the expression of Parkin protein in Hvh,Hh,Hm,Hl group decreased,but there was no significant difference in O₂ group.There was no significant difference in the expression of PINK1protein among the groups.Conclusions:1 Inhalation of hydrogen reduces lung pathological damage.Different concentrations of hydrogen have different effects.Medium,high,and extremely high concentrations are superior to low concentrations of hydrogen.2 Hydrogen can delay the development of COPD through antioxidation.3 Hydrogen may delay COPD progression through mitochondrial autophagy.