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Effects of Qiaojing Compound Preparation on Cardiomyopathy in Rats Model Induced by Type 2 Diabetes Mellitus

Author: LiJie
Tutor: BaoJuTai
School: North China Coal Medical
Course: Chinese medical science
Keywords: Diabetes Cardiomyopathy The buckwheat fine compound preparation Tumor Necrosis Factor
CLC: R285.5
Type: Master's thesis
Year: 2010
Downloads: 35
Quote: 0
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Abstract


Background: Diabetes mellitus (DM, Diabetes mellitus) as a common and frequently-occurring disease, they cause various complications caused major cause of death in patients with diabetes. Diabetic cardiomyopathy (DCM, Diabetic cardiomyopathy) is one of the most serious complications of diabetes, it refers to the primary injury of diabetic patients with myocardial cells caused extensive structural abnormalities, eventually causing left ventricular hypertrophy, diastolic and (or) contraction Doctors can only take symptomatic treatment, regulation of Chinese medicine as a whole has a lot of advantages in the prevention and treatment of complications of diabetes, can play a role in treatment of both specimens, therefore, to seek safety in Chinese medicine for the treatment of diabetes and its complications has important significance. We found in the early experimental studies buckwheat total flavonoids hypoglycemic, and lipids, improve glucose tolerance, and there is a strong antioxidant and free radical scavenging effects. The experimental study was conducted on this basis with buckwheat grass plus Polygonatum, habitat TCD buckwheat fine compound preparation (QJCP), high fat diet combined chain STZ model of type 2 diabetes, The intervention treatment during the experiment using QJCP Description QJCP diabetic cardiomyopathy role, aimed at the study the QJCP of type 2 diabetes and its myocardial damage and to explore the possible mechanism by objective indicators of change. Purpose: a high fat diet plus chain STZ (streptozotocin, STZ)-induced type 2 diabetes model in rats with QJCP intervention to observe QJCP cardiomyopathy in diabetic rats, and to explore the possible mechanisms. Methods: 1. Establishment of animal model: healthy male SD rats, adaptive feeding after a week, randomly selected 12 as the normal control group (NC), normal diet. The remaining rats fed with high fat diet for four weeks after intraperitoneal injection of STZ 30mg/kg 7 days after re-injection of the same method to establish a rat model of diabetes, fasting plasma glucose ≥ 11.1mmol / L or more, while glucose tolerance (rat intragastric glucose 2g/kg, detection at 120 min) 120min blood glucose levels higher than 20% of the value of fasting glucose as modeling success indicators. Animal grouping and dosing regimen selected modeling success rat 53, were randomly divided into four groups: model control group (MC) 13, distilled water; buckwheat fine compound preparation of the high-dose group (QJCPH), low-dose group ( QJCPL) 14 each the, QJCP dose were 1.2g/kg and 0.6g/kg; Xiaoke Pill group (XKW) 12 and Xiaoke pill dose 0.83g/kg; these groups with high fat diet feeding; normal control group distilled water, and fed with normal diet. The five groups were orally once a day, for eight weeks. Indexes ① observed the general condition of the rats (coat color, spirit, diet, drinking water, urine output, etc.); ② glucometer fasting blood glucose (FBG); ③ colorimetric determination of serum total cholesterol (T-CHO), glycerol three ester (TG) and free fatty acid (FFA); ④ put free method determination of serum tumor necrosis factor (of TNF-α) level; ⑤ detection rats the heart weight index (HWI = HW / BW, that heart weight index = heart weight / body weight ); ⑥ myocardial tissue HE staining, light microscope, the pathological changes of the myocardium were observed and analyzed; ⑦ immunohistochemical determination of myocardial TNF-α protein expression; the ⑧ electron microscopy myocardial ultrastructure change; Results: 1 the general condition of the model group rats lassitude, curled up, lack of exercise, the body hair dull, increased water intake, increased urine; improve the general condition of each dose group in varying degrees. 2. QJCP affect model rats rats fasting glucose fasting plasma glucose was significantly higher than the normal group (P lt; 0.01); compared with the model group, the drug treatment group was significantly lower (p lt; 0.01). The 3. QJCP serum lipids with the normal group compared with the model group of cholesterol, triglycerides and free fatty acids were significantly higher (P lt; 0.01), QJCP treatment group were significantly lower than the model group ( p lt; 0.01). 4. QJCP serum TNF-α levels can be seen from the results in the model group was significantly higher than the normal group (P lt; 0.01), compared with the model group, QJCP treatment serum TNF-α levels significantly lower The best QJCPH treatment group (P lt; 0.01). 5. QJCP diabetic rat heart weight index results show that the model group and normal control group compared heart weight index were significantly different (P lt; 0.01) QJCP treatment of heart weight index has declined the most obvious, QJCPH treatment group ( P lt; 0.01). 6. QJCP myocardial pathological changes observed by light microscopy model rats myocardial fibers disorganized, cardiomyocyte hypertrophy, cell gap increases, visible muscle fiber breakage, and inflammatory cell infiltration. Myocardial pathological changes of the treated rats was significantly improved, QJCPH treatment group was close to normal rat cardiac tissue structure. 7. QJCP impact on myocardial TNF-α protein expression by immunohistochemical staining: model rats myocardial TNF-α protein was highly expressed in myocardial tissue visible brown dyed myocardial TNF and QJCPH treated rats -α protein showed low expression, a small amount of brown-yellow staining in the myocardial tissue. Affect model rats the QJCP ultrastructural changes in rat cardiomyocytes appear the myofilaments focal myocardial cells dissolved Ming band broadening sarcomere loss of normal structure, mitochondrial swelling, mitochondrial cristae structure sparse arrangement to reduce or disappear. Compared with the model group, the ultrastructural changes QJCPH treatment of myocardial cells significantly reduced. Conclusion: QJCP has a certain extent of myocardial damage in STZ-induced diabetic rats. The mechanism may be related to lower blood sugar, regulate blood lipids, and inhibit the production of tumor necrosis factor.

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