| Objective: In recent years, the incidence of diabetes is rising.Caused by diabetes, the incidence of heart failure is significantly higher than non-diabetic patients with elevated. Diabetic cardiomyopathy(DC)may play a key role in the process of diabetes promoting heart failure. Myocardial fibrosis, myocyte apoptosis plays an important role in the development and progression of diabetic cardiomyopathy promote. This article will use α-smooth muscleaction(α-SMA) to demonstrate the presence of the gene expression of myocardial fibrosis in diabetic cardiomyopathy by cardiac pathology and cardiac tissue, and explore the pathology of cardiac tissue from diabetic state P53 gene expression the impact of changes.Benazepril, which plays its role through angiotensin converting enzyme,belongs to angiotensin converting enzyme inhibitors( ACEI) class of antihypertensive drugs and has a good ability to controlling blood pressure. Recent studies have found that benazepril also by inhibition of the renin- angiotensin system( RAS), reducing reactive oxygen species( ROS) generation of excessive delay atherosclerosis progress, and can reduce oxidative stress, improve endothelial function and reduce the inflammatory cell activity. Whether it could improve glucose Prognosis diabetes cardiomyopathy patients, and their associated possible mechanism or not is still uncertain.This trial will take streptozotocin(STZ) induced by intraperitoneal injection of a diabetic rat model, be benazepril orally on this basis, to observe the expression of myocardial tissue P53, α-SMA gene m RNA. Methodology: 1.Animal grouping and processing test specimensIn this study, rats were divided into three groups: control group, diabetic group, benazepril group. The specific test method:Male SD rats 8 weeks 42, weighing 200-220 g, adaptive feeding about a week, then 12 divided into control group, the experimental group 30. Blank control group were given free access to food water, the experimental group were fasted for 12 hours after a single intraperitoneal injection of 2% STZ65mg/kg; injection 72 hours after harvest tail vein blood glucose, blood glucose> 16.5mmol / L for the success of the standard model. For statistical modeling and removal of the failed model, the model is successful in diabetic SD rats were randomly divided into 12 groups, benazepril group 12, the two groups were fed ad libitum feeding water eight weeks, eight weeks later, benalapril group were given daily hydrochloride tablets 10mg/kg orally intervention control group and diabetes group fed normal saline solution. Until 8 weeks the rats were sacrificed. After each group of mice were sacrificed before fasting for 12 hours and be 25% urethane 6ml /kg,intraperitoneal injection, quickly open the chest and remove the rat heart, minus the blood vessels and heart tissue surrounding rinsed with saline and gauze absorb moisture weighing surface of the heart. After weighing each take a little rat apical tissues were placed paraformaldehyde solution in order to make the line HE biopsy. The rest of myocardial tissue cryopreservation placed at-80 ℃ for later extraction of total RNA, measured the expression of myocardial tissue P53, α-SMA gene m RNA. 2.Rat tail vein blood glucose :Using Oxidase method. 3.Myocardial slice production: With hematoxylin- eosin( HE) staining in SD rat myocardium slices. 4.measuring the expression of myocardial tissue P53, α-SMA gene m RNA. : Trigol myocardial extraction method of total RNA, with GADPH as internal control, real fluorescence quantitative PCR(the abbreviation for reverse transcript-q PCR, RT-q PCR) assay using reverse transcription when the relative expression of cardiac P53, α-SMA gene m RNA. 5.Data Processing: In this study, all data were X ± s said, using SPSS15.0 software for statistical analysis, each group using pairwise t test, with α = 0.05 for the test, with P <0.05 was considered statistically significant. Results: 1.Manufacturing animal model. 1.1Diabetic rats and benazepril blood sugarAfter intraperitoneal injection of STZ these two groups to be 72 hours, taking blood glucose test rat tail, removing the modeling of failure, the remaining rats were in line with the standard type 1 diabetes, and accompanied by polydipsia and polyuria eating symptoms. This had showed the success of producing modles. 1.2Weight, body mass index, heart weight and heart of ratsModeling after 16 weeks the rats were weighing and sacrificed, then measuring heart weight.compared with the control group’s body weight and heart weight, two groups of rats were decreased(P <0.05), but the heart of the body mass index than the control group liter high(P <0.05). Diabetic group and benazepril group showed no statistically significant above. 2.HE staining of myocardial:Control group HE staining of myocardial muscle fibers arranged in neat rows and stripes clearer nucleus into a round, oval, stained lighter, no cell swelling. Compared with the control group, diabetic group had showed hypertrophy of muscle fibers, and the disorganized, and myocardial fiber breakage, nuclei stained deeper than the control group, and the increase in the number of nuclei under the same vision, irregular nucleus, nuclear size heterogeneity. 3.The expression of myocardial tissue P53, α-SMA gene m RNA.Compared with the control group’s body weight the expression of diabetic myocardium tissue P53 and α-SMA gene increased, the difference was statistically significant(P <0.05); compared with the diabetic group, benazepril myocardial tissue P53, α-SMA gene expression is reduced, the difference was statistically significant(P <0.05). Conclusions: 1.comparison with the control group’s body weight,diabetic groups of rats were decreased,the heart of the body mass index than the control group liter high. 2.The expression of myocardial tissue of diabetic rats compared with P53 gene m RNA in the control group increased;After diabetic rats by benazepril intervention with respect to the expression of the diabetic group, benazepril group P53 gene m RNA is reduced. 3.The expression of myocardial tissue of diabetic rats compared with α-SMA gene m RNA in the control group increased;After diabetic rats by benazepril intervention with respect to the expression of the diabetic group, benazepril group α-SMA gene m RNA is reduced. |
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