Found programs:
Authors:Gao Xiang; Liu Kou; Gui Yanchao
Keywords:diabetic retinopathy;captopril;cholesterol;triglycerides;sterol regulatory element binding protein 1;sterol regulatory element binding protein 2
DOI:10.19405/j.cnki.issn1000-1492.2021.04.017
〔Abstract〕 Objective To investigate the effect of captopril on lipid metabolism in diabetic mellitus(DM) rats and its relationship with diabetic retinopathy(DR). Methods Thirty male SD rats aged 8 weeks were randomly divided into normal control group(n=10) and model group(n=20). The model rats were induced by high-fat diet(HFD) combined with streptozotocin(STZ) to establish the model of type 2 diabetes mellitus rats. The model rats were randomly divided into captopril group(DM+CAP) and normal saline group(DM+NS) with 10 rats in each group. Rats in DM + CAP group were gavaged with captopril 25 mg/(kg·d), and DM+NS group were gavaged with equal volume normal saline. Body weight and fasting blood glucose were measured weekly. After 8 weeks of intervention, the rats were euthanized, the whole blood was collected, serum was separated and retinal tissue was collected. The concentrations of total cholesterol(TC) and triglyceride(TG) in serum were detected; the structure of retina was observed, including the structure changes of inner and outer nuclear layers, and the number of new blood vessels; the levels of cholesterol regulatory element binding protein 1(SREBP1) and cholesterol regulatory element binding protein 2(SREBP2) were detected. Results Captopril could not reduce fasting blood glucose in rats. Compared with DM+NS group, the concentration of TC and TG in serum of DM+CAP group decreased(P<0.01); the retinal tissue structure improved: the inner and outer nuclear layer cells were tightly connected, the number of new blood vessels was less; the expression levels of SREBP1 and SREBP2 decreased(P<0.01). Conclusion Captopril can reduce the blood lipid related indexes of diabetic rats, improve the retinal tissue morphology, and reduce the key enzymes of lipid synthesis in the retina of diabetic rats. The mechanism may be related to its inhibition of lipid synthesis.