Captopril In The Treatment Of Diabetic Retinopathy By Inhibiting Oxidative Damage And Dyslipidemia

Objective Many studies have suggested that captopril has a positive therapeutic effect on diabetic retinopathy(DR),but the mechanism has not been clearly elucidated.Oxidative damage and dyslipidemia play important roles in the pathogenesis of DR.This study wanted to explain the relationship between the therapeutic effect of captopril and oxidative damage and dyslipidemia in DR.Methods Through the outpatient and inpatient department to determine the patient information,collect the patient blood routine report and related indicators of this topic,sort out the records.Diabetic mice(DM)were randomly divided into two groups that were treated as follows: 25 mg/kg/day captopril solution or an equal volume of normal saline was given by tube feeding.All mice were fed normal feed and drinking water for12 weeks.Human retinal microvascular endothelial cells(HRMECs)were cultured in5.5 m M or 30 m M glucose medium and treated with 1 m M or 2 m M captopril for 24 h.Fasting plasma glucose,body weight,24-h food intake and 24-h water intake of mice were measured regularly.The structure and neovascularization of the mouse retina were observed by HE staining and Evans blue angiography.The levels of TC,TG,and NO in mice and HRMECs were examined by assay kits.The expression levels of SREBP1,SREBP2,e NOS,i NOS,and VEGF in the retinas of mice and HRMECs were examined.Results Clinical data showed that compared with Dr patients who did not take captopril,the levels of TC,TG and no in blood samples of Dr patients who took captopril were lower.Compared with the untreated mice,the weight and 24-h food intake of the captopril treated mice decreased at 7-12 weeks and 11-12 weeks respectively,and there was no significant difference in blood glucose and water intake between the two groups;compared with the normal control mice,the blood glucose,weight,food intake and water intake of the T2 DM mice increased.The retinal structure and neovascularization were obviously improved by captopril.The TC,TG,and NO levels in diabetic mice and HRMECs cultured in medium containing 30 m M glucose were increased,while captopril reduced the above parameters.The expression levels of SREBP1,SREBP2,i NOS,and VEGF were upregulated but e NOS was downregulated after 30 m M glucose stimulation in HRMECs or diabetic retinal tissue.Interestingly,the expression levels of the above markers were inverted following captopril intervention.Conclusions The study found that captopril can reduce the oxidative damage of DR by reducing the concentration of NO,inhibiting the formation of peroxynitrite and regulating the disorder of lipid metabolism.