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Effects of Atorvastatin on Myocardiocyte Apoptosis and ROS after Acute Myocardial Infarction in Rats

Author: QinZhiPing
Tutor: LiuZongFang
School: Zhengzhou University
Course: The prevention and treatment of coronary heart disease
Keywords: Atorvastatin Ventricular remodeling Cardiomyocyte apoptosis ROS Oxidative Stress P53
CLC: R542.22
Type: Master's thesis
Year: 2007
Downloads: 200
Quote: 1
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Abstract


Background and purpose in recent years, with acute myocardial infarction (acute myocardial infarction, AMI) has become one of the serious threat to human health, disease, and left ventricular remodeling after AMI is the main reason for patients with heart failure. Ventricular remodeling is caused by a complex series of molecular and cellular mechanisms of myocardial cell structure, function and phenotypic changes. Cardiomyocyte apoptosis induced early and late remodeling recently received increasingly widespread attention. Apoptosis by a variety of signaling molecules involved in multifactorial regulation of cell active death process. Oxidative stress (oxidative stress, OS) has been shown to induce apoptosis in many cell types in culture, is considered to be the common medium of apoptosis, reactive oxygen species (reactive oxygen species, oxidative stress ROS) mediated apoptosis can be used as a signal molecule. But the ROS how-mediated apoptosis is unclear, a number of studies have shown that P53 increased expression of ROS-mediated apoptosis, and activation of downstream signaling molecules, may be involved in the signal transduction process. Outside the role of statin anti-inflammatory, antioxidant lipid has some degree of certainty, but the impact of his class of statins on apoptosis mixed results, whether statin inhibition of cardiomyocyte apoptosis by the antioxidant role still unclear, for this study, to select 3rd generation statins Alto atorvastatin, observe the AMI rat model of myocardial tissue content of ROS, P53mRNA expression levels and myocardial apoptosis, analysis of the correlation between these indicators relationship, explore the ventricular remodeling process in the role of oxidative stress in myocardial apoptosis and atorvastatin statin intervention of its impact, to further elucidate the molecular mechanisms of ventricular remodeling, and provide experimental basis for the inhibition or reversal of ventricular remodeling. Materials and methods. The modeling packet healthy and clean 65 male Wistar rats, weighing 240 ± 20g, were randomly divided into sham group (n = 15) and AMI group (n = 50); AMI group by ligation of the left anterior descending coronary artery ( left anterior descending branch, LAD) production of AMI model, successful 24h survival after 36, and then randomly divided into the atorvastatin intervention group (n = 18) and myocardial infarction in the control group (n = 18). Atorvastatin statin intervention group with Atto cutting statins 40mg/kg orally daily with normal saline control group and the sham group of myocardial infarction gavage for 4 weeks. 2. Echocardiographic evaluation of left ventricular function using two-dimensional echocardiography probe frequency of 10MHz, long fetch standards left ventricular short axis view, respectively, perioperative determination of left ventricular diastolic diameter (left ventricular end-diastolic diameter, LVEDd) Left ventricular ejection fraction (left ventricular ejection fraction, LVEF) and left ventricular shortening fraction (fractional shortening, FS). 3. The ROS detection fetch rats non-infarcted myocardial tissue preparation homogenates, colorimetry samples superoxide anion (O 2 - ·) and hydroxyl radical (OH ·) content were measured . 4. Rats myocardial tissue the P53mRNA detection sterile conditions to remove RNA enzyme collecting non-infarcted myocardial tissue of rats in each group of SYBR Green I real-time quantitative PCR assay specimens P53mRNA expression. Housekeeping gene GAPDH as an internal, compared to the quantitative results of the quantitative results of the P53 gene in each sample and GAPDH gene correction, relative quantitative analysis of myocardial tissue of rats P53mRNA expression. 5. Determination of myocardial apoptosis index (apoptosis index, AI) take non-infarcted myocardium tissue using terminal deoxynucleotidyl transferase-mediated biotin nick end labeling (TdT-mediated dUTP nick end labeling, TUNEL) assay myocardial cells apoptosis, calculate the apoptosis index. Results 1. General: After four weeks, the rats survival were: the atorvastatin the statin intervention group 14, control group of 13 myocardial infarction, 14 sham group. 3 rats weight significantly (P> 0.05); atorvastatin Ting intervention group and myocardial infarction control rats, heart weight, left ventricular weight, heart weight index and left ventricular mass index were significantly higher than the sham group (P <0.05), while atorvastatin statin intervention group above indicators significantly lower than the Myocardial Infarction control group (P <0.05). 2. Left ventricular function: 4 weeks after echocardiography showed left ventricular cardiac function: atorvastatin The Ting intervention group and myocardial infarction control group LVEDd significantly higher than the sham group (P <0.05), and the LVEF and FS was significantly lower than the sham group (P <0.05); compared to the control group with myocardial infarction, atorvastatin the statin intervention group LVEDd significantly lower (P <0.05), LVEF and FS significantly higher (P <0.05 ). 3. ROS, P53 mRNA and myocardial apoptosis: atorvastatin Ting intervention group and myocardial infarction in rats in the control group compared to the sham group, the non-infarcted myocardium superoxide anion (O 2 - · ) and hydroxyl radical (OH ·) content, the amount of P53 mRNA expression and myocardial cell AI were significantly higher (P <0.05); while atorvastatin statin intervention group rats in the non-infarcted myocardium superoxide anion (O < sup> 2 - ·) and hydroxyl radical (OH ·) content, the amount of P53 mRNA expression and apoptosis index were significantly lower than the control group of myocardial infarction (P <0.05). 4. Pearson linear regression analysis: atorvastatin statin intervention group and myocardial infarction control rats in the non-infarcted myocardium superoxide anion (O 2 - ·) of the content, the amount of P53 mRNA expression of myocardial cells withered between death index were positively correlated (P <0.05). Conclusion 1. Increased cardiomyocyte apoptosis after myocardial infarction, left ventricular function decline; atorvastatin reduces myocardial apoptosis index, improved left ventricular function. 2. ROS (superoxide anion (O 2 - ·) and hydroxyl radical (OH ·)) content and P53mRNA of expression were increased in the non-infarcted myocardium 4 weeks after myocardial infarction in rats Atorvastatin in its expression can be suppressed to a certain extent. 3. ROS and p53 genes involved in the process of cardiomyocyte apoptosis after myocardial infarction. 4. Atorvastatin reduced myocardial tissue ROS (superoxide anion (O 2 - ) and hydroxyl radical (OH ·)) content and P53mRNA of expression may be its suppression after myocardial infarction myocardial cells wither one of the mechanism of death, improve heart function.

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Myocardial diseases > Myocardial infarction
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