Intermittent Hypoxia Induced Myocardial Injury In Rats And The Intervention Of Edaravone

Objective: To establish a model of chronic intermittent hypoxia(CIH)to simulate the occurrence of obstructive sleep apnea hypopnea syndrome(OSAHS)in adults,to explore the relationship between oxidative stress,β-catenin expression and CIH-induced myocardial fibrosis,observe the effect of edaravone on CIH-induced myocardial fibrosis injury,in order to provide new research directions for myocardial fibrosis and myocardial remodeling caused by OSAHS.Methods: Establish an intermittent hypoxia model: Selecting 4-week-old healthy male Sprague-Dawley(SD)rats,fed with ordinary diet to 8 weeks of age,and divided them into 4 groups using a random number table method,the following is the group:the first group: Normal control group;the second group: CIH group;the third group:CIH+ normal saline group;the fourth group: CIH+ edaravone group.The first group was kept in a room with a normal environment and temperature,during which time they could eat and move freely;the other three groups were placed in an intermittent hypoxic chamber during the experimental period,and the non-experimental time was the same as the first group.The duration of intermittent hypoxia modeling was 8hours a day for 8 weeks.After the modeling(ie 57 th day),taking heart specimens from each group of rats to prepare slices,observing the morphological changes of myocardial tissue by hematoxylin-eosin(H&E)staining and Masson staining under light microscope;detect the levels of LDH,CK,CK-MB in rat serum and SOD,GSH-Px and MDA content in myocardial tissue;immunohistochemical method was used to detect the expression of β-catenin in myocardial tissue.Results: 1.Compared with the NC group,the arrangement of myocardial cells in the CIH group and the CIH+NS group was disordered,the vertical and horizontal lines were unclear,the muscle fiber rupture,degeneration,and necrosis were seen locally,the myocardial space was significantly widened,and more collagen fiber deposition was seen in the myocardial space.The degree of myocardial fibrosis increased significantly;2.Compared with NC group,serum LDH and CK-MB levels in CIH group and CIH+NS group increased(P<0.05),SOD and GSH-Px levels in myocardial tissue decreased(P<0.01),the content of MDA increased(P<0.01);but the change of CK level was not statistically significant among the groups;3.Compared with the NC group,the expression of β-catenin in the cytoplasm and nucleus of the CIH group and the CIH+NS group was significantly increased(P<0.01);4.After administration of edaravone,rat myocardial tissues could be observed the structural disorder of the disease is weaker than before,the serum levels of LDH and CK-MB are significantly lower than before(P<0.01),the contents of SOD and GSH-Px are significantly increased(P<0.01),and the content of MDA and the expression of β-catenin decreased(P<0.01).Conclusion: 1.Chronic intermittent hypoxia exposure can cause structural disorders in rat cardiomyocytes and fibrotic changes in the interstitium of cardiomyocytes;2.Chronic intermittent hypoxia exposure increases the level of peroxides in myocardial tissue,decreases the level of antioxidants,and increases the expression of β-catenin;3.Edaravone may reduce myocardial fibrosis induced by intermittent hypoxia by inhibiting the level of oxidative stress and the expression ofβ-catenin.