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find Keyword "Nicotinamide adenine dinucleotide phosphate oxidase" 2 results
  • EFFECTS OF TYPE 2 DIABETES MELLITUS ON THE STRUCTURE AND OXIDATIVE STRESS IN GREAT SAPHENOUS VEIN GRAFTS

    Objective To compare the condition of the structure and oxidative stress of great saphenous vein grafts between the patients with and without type 2 diabetes mellitus, and to study the mechanisms for providing the theory evidence ofthe protective way for great saphenous vein graft in patients with type 2 diabetes mellitus. Methods The segments of human great saphenous vein graft were collected from 36 patients undergoing coronary artery bypass graft surgery, who were divided into 2 groups, experimental group (17 patients with type 2 diabetes mellitus) and control group (19 patients without type 2 diabetes mell itus). There was no significant difference in age, gender, hypertension, serum creatinine, hyperl ipidemia, smoking, and the number of pathological coronary arteries between 2 groups (P gt; 0.05). Two cm distal great saphenous vein from each patient was obtained. The structure of great saphenous vein was observed by the microscope, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzymatic activity and superoxide anion level were quantified by lucigenin-enhanced chemilumi nescence. Results The NADPH oxidase activity and superoxide anion levels were significantly higher in experimental group [(308.8 ± 33.7) counts/μg and (1 951.71 ± 355.2) counts/(min.mg)] than in control group [(202.7 ± 29.5) counts/μg and (1 230.73 ± 340.5) counts/(min.mg)] (P lt; 0.05). HE staining showed the damage of ultrastructure of great saphenous vein endothel ium in experimental group, including necrosis and exfol iation of endoepithel ial cells, spl itting of the basement membrane, thickened lower layer of the endothelium with vacuoles and deformed vascular smooth muscle cells; however, integrated vessel intima was observed in control group.

    Release date:2016-08-31 05:43 Export PDF Favorites Scan
  • Protective Effect of Roux-en-Y Gastric Bypass Surgery on Early Damage of Renal Tissue in Type 2 Diabetes Mellitus Rats

    ObjectiveTo investigate the protective effect of Roux-en-Y gastric bypass surgery on early damage of renal tissue in type 2 diabetes mellitus rats, and explore the mechanism of the protective effects. MethodsDiabetes mellitus animal models were induced by intraperitoneal injection of streptozotocin (STZ, 35 mg /kg) and a high-fat diet.Diabetic rats were divided into three groups randomly (digital table method): diabetes control group (n=8), sham operation group (n=8), and Roux-en-Y gastric bypass group (n=14).Another 8 normal SD rats as the normal control group.The fasting blood glucose, serum total cholesterol (TC), triglyceride (TG), and free fatty acid (FFA) were measured before operation and in 8 weeks after operation; plasma BUN and Cr were measured respectively before operation and in 4 and 8 weeks after operation in each group rats, 24 h urine microalbumin and urine 8-hydroxydeoxyguanosine were measured respectively before operation and in 8 weeks after operation in each group rats.Renal pathological changes were observed and the indexes of kidney hypertrophy, the mean glomerular area (MGA), and the mean glomerular volume (MGV) were analyzed in 8 weeks after operation.The expressions of fibronectin, typeⅣcollagen (CoⅣ), transforming growth factor-β1 (TGF-β1), intercellular adhesion molecule-1(ICAM-1), nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), and Bcl-2 protein in renal tissues were investigated by immunohistochemical staining. ResultsRoux-en-Y gastric bypass surgery could reduce the blood glucose, blood lipid, MGA, MGV, and the index of kidney hypertrophy of diabetic rats significantly (P < 0.05), improved renal pathological morphology and kidney function (P < 0.05), reduced the protein expressions of fibronectin and CoⅣ, decreased the protein expressions of TGF-β1, ICAM-1, and NOX4, and increased the protein expression of Bcl-2. ConclusionRoux-en-Y gastric bypass surgery can improve kidney function and the pathological damage of diabetes rats, its mechanism may be related to inhibition the protein expressions of TGF-β1, ICAM-1, and NOX4, and increase the protein expression of Bcl-2.

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