本文關(guān)鍵詞： 丁基苯肽 冠狀動(dòng)脈結(jié)扎 線粒體損傷 細(xì)胞凋亡 凋亡指數(shù) 心肌梗死　出處：《安徽醫(yī)科大學(xué)》2014年碩士論文　論文類型：學(xué)位論文

【摘要】：研究背景和目的NBP在急性腦卒中過程中，具有提高大腦能量代謝，抗氧化作用，促進(jìn)微循環(huán)，減少神經(jīng)細(xì)胞凋亡以及抑制炎癥反應(yīng)的作用。NBP同樣被證明可減少內(nèi)皮細(xì)胞缺氧誘導(dǎo)的線粒體活性氧(Reactive oxygen species ROS)的形成，減輕由急性缺氧導(dǎo)致的超氧化物歧化酶(superoxide dismutase, SOD)的活性的降低，減少線粒體損傷以及線粒體膜電荷的損失，保護(hù)線粒體結(jié)構(gòu)和功能的完整性，進(jìn)而降低神經(jīng)細(xì)胞網(wǎng)凋亡和急性腦卒中引起的大腦梗死面積。所以本將觀察丁基苯酞對大鼠心肌梗死后對心肌細(xì)胞線粒體，心肌梗死面積及心肌細(xì)胞凋亡的作用。 研究方法共64只雄性SD大鼠，分為假手術(shù)組8只，模型組、實(shí)驗(yàn)組各28只。用大豆油溶解丁苯酞液體（將丁苯酞稀釋在食用油大豆油制成8mg/ml的丁苯酞溶液備用，按80mg/kg灌胃），實(shí)驗(yàn)組對大鼠灌胃丁苯酞溶液，其余兩組均只灌胃大豆油，每日2次，每次1ml/100g。以上各組灌胃飼養(yǎng)一周后制備心肌梗死模型。其中模型組和實(shí)驗(yàn)組需通過結(jié)扎冠狀動(dòng)脈左前降支建立MI模型，假手術(shù)組僅開胸，未結(jié)扎冠狀動(dòng)脈。模型組和實(shí)驗(yàn)組分別于結(jié)扎冠脈后1h、4h、8h和12h取心臟標(biāo)本，，每個(gè)時(shí)間點(diǎn)7只大鼠。TUNEL法檢測實(shí)驗(yàn)大鼠AMI過程梗死交界區(qū)心肌細(xì)胞凋亡。各組取心肌組織應(yīng)用TTC染色分析心肌梗死面積，電子透射顯微鏡觀察4h后各組梗死交界區(qū)的心肌細(xì)胞的超微結(jié)構(gòu)，根據(jù)樣本線粒體的損傷程度，評估整體線粒體得分。Western-bloting法檢測大鼠心肌梗死4h后Bcl-2、Bax的蛋白含量，計(jì)算Bcl-2/Bax的比值。 研究結(jié)果與模型組相比，在大鼠急性心肌缺血過程中，丁基苯肽可有效抑制線粒體損傷；同時(shí)急性心肌梗死后12h丁基苯酞可顯著減少大鼠急性心肌梗死面積(P0.05)；丁苯酞可顯著減少心肌細(xì)胞凋亡(P0.05)。丁苯酞可明顯改善線粒體損傷丁基苯肽顯著提高Bcl-2蛋白表達(dá)水平及Bcl-2/Bax的比值。 研究結(jié)論丁基苯肽可顯著提高Bcl-2蛋白表達(dá)水平及Bcl-2/Bax的比值，減少線粒體損傷，降低心肌梗死過程中細(xì)胞凋亡指數(shù)，縮小心肌梗死面積，具有顯著地心肌保護(hù)效應(yīng)。
[Abstract]:Background and objective NBP plays an important role in improving brain energy metabolism, antioxidant activity and microcirculation during acute stroke. NBP has also been shown to reduce mitochondrial reactive oxygen species (Ros) induced by hypoxia in endothelial cells. The formation of Reactive oxygen species ROS. It can reduce the activity of superoxide dismutase (SOD) induced by acute hypoxia, and reduce the damage of mitochondria and the loss of membrane charge. Protect the integrity of mitochondria structure and function, and then reduce apoptosis of neural network and cerebral infarction area caused by acute cerebral apoplexy. Therefore, we will observe the effect of Ding Ji phthalide on myocardial mitochondria after myocardial infarction in rats. The effect of myocardial infarction area and cardiomyocyte apoptosis. Methods 64 male SD rats were divided into sham-operated group (n = 8) and model group (n = 8). The experimental group (n = 28) was dissolved in butadiphthalein liquid with soybean oil (8mg / ml butylphthalide solution was prepared by dilution of butylphthalide in edible oil soybean oil, and was perfused by stomach at 80 mg / kg). The rats in the experimental group were given butyphthalide solution, and the other two groups were only given soybean oil twice a day. Myocardial infarction model was established in each group of 1 ml / 100 g. The model group and experimental group need to establish MI model by ligating the left anterior descending coronary artery, and the sham operation group only opened the chest. No coronary artery was ligated. The heart samples were taken from the model group and the experimental group at 1 hour after coronary artery ligation for 8 h and 12 h, respectively. Tunel method was used to detect myocardial cell apoptosis in the infarct junctional area of experimental rats during AMI at each time point. Myocardial tissue was taken from each group to analyze myocardial infarction area by TTC staining. Electron transmission microscope was used to observe the ultrastructure of myocardial cells in each group after 4 hours, according to the damage degree of mitochondria. The total mitochondrial score. Western-blotting method was used to detect the protein content of Bcl-2P Bax and calculate the ratio of Bcl-2/Bax in rats with myocardial infarction 4 h after myocardial infarction. Results compared with the model group, Ding Ji benzopeptide could effectively inhibit mitochondrial damage during acute myocardial ischemia in rats. At the same time, 12h after acute myocardial infarction, Ding Ji phthalide could significantly reduce the area of acute myocardial infarction (AMI) in rats (P 0.05). Butyphthalide could significantly reduce cardiomyocyte apoptosis (P 0.05). Butyphthalide could significantly improve the expression level of Bcl-2 protein and the ratio of Bcl-2/Bax to Bcl-2/Bax after mitochondrial injury of Ding Ji. Conclusion Ding Ji benzopeptide can significantly increase the expression level of Bcl-2 protein and the ratio of Bcl-2/Bax, reduce mitochondrial damage and decrease apoptosis index during myocardial infarction. Reducing myocardial infarction size has significant myocardial protective effect.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R542.22

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相關(guān)期刊論文 前1條

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