本文選題：心肌缺血再灌注損傷 + 穩(wěn)心丹��； 參考：《黑龍江中醫(yī)藥大學(xué)》2017年博士論文

【摘要】：目的:探討穩(wěn)心丹不同配伍比例對(duì)心肌缺血再灌注損傷模型大鼠的心肌保護(hù)作用及相關(guān)抗炎機(jī)制。方法:1.將70只SD大鼠隨機(jī)分為7組,即模型組、假手術(shù)組、預(yù)處理組、穩(wěn)心丹1:1:1組、穩(wěn)心丹1:2:1組、穩(wěn)心丹1:1:2組、穩(wěn)心丹2:1:1組,分別作用于心肌缺血再灌注損傷模型大鼠,檢測(cè)其對(duì)模型大鼠血清CK-MB、cTnI的含量及心肌梗死面積的影響;進(jìn)行穩(wěn)心丹配伍比例關(guān)系量化考查,選出最優(yōu)配伍比例組。2.運(yùn)用透射電鏡觀察穩(wěn)心丹對(duì)心肌缺血再灌注損傷模型大鼠的心肌超微細(xì)結(jié)構(gòu)的影響,免疫組化法檢測(cè)穩(wěn)心丹對(duì)心肌組織中T-Akt、p-Akt的表達(dá)的影響。從而探討穩(wěn)心丹抗心肌缺血再灌注損傷的作用機(jī)制。3.通過免疫印跡法、免疫組化法檢測(cè)穩(wěn)心丹對(duì)心肌缺血再灌注損傷模型大鼠心肌組織中NF-κB、COX-2的蛋白分布及表達(dá)的影響。4.觀察穩(wěn)心丹對(duì)心肌缺血再灌注損傷模型大鼠血清中TNF-α、IL-1β、IL-6、IL-10含量的影響,探討其抗炎作用機(jī)制。結(jié)果:1.穩(wěn)心丹各治療組均能夠明顯降低心肌缺血再灌注損傷模型大鼠血清中CK-MB、cTnI含量、使MIRI模型大鼠心肌梗死面積減小,其中穩(wěn)心丹1:2:1組效果最為顯著。2.穩(wěn)心丹1:2:1組與模型組比較可顯著改善心肌缺血再灌注損傷模型大鼠的心肌超微細(xì)結(jié)構(gòu);提高心肌組織p-Akt蛋白表達(dá)。3.穩(wěn)心丹1:2:1組與模型組比較可顯著抑制心肌缺血再灌注損傷模型大鼠心肌組織中NF-κB、COX-2的蛋白分布及表達(dá)。4.穩(wěn)心丹1:2:1組與模型組比較可顯著降低心肌缺血再灌注損傷模型大鼠血清中TNF-α、IL-1β、IL-6的含量,升高IL-10的含量。結(jié)論:1.穩(wěn)心丹不同配伍比例組均能明顯降低心肌缺血再灌注損傷模型大鼠心肌酶CK-MB、cTnI含量,使MIRI模型大鼠心肌梗死面積減小,選出抗心肌缺血再灌注最佳配伍比例組為穩(wěn)心丹1:2:1組。2.穩(wěn)心丹通過激活PI3K/Akt信號(hào)轉(zhuǎn)導(dǎo)通路,提高心肌組織p-Akt蛋白表達(dá),減少NF-κB、Cox-2蛋白表達(dá),減輕心肌組織損傷程度,發(fā)揮心肌保護(hù)作用。3.穩(wěn)心丹通過激活PI3K/Akt信號(hào)轉(zhuǎn)導(dǎo)通路,下調(diào)炎癥因子TNF-α、IL-1β、IL-6表達(dá),并能夠促進(jìn)抑炎因子IL-10釋放,進(jìn)而發(fā)揮心肌保護(hù)作用。
[Abstract]:Aim: to investigate the protective effect of Wenxindan (WXD) on myocardium in rats with myocardial ischemia reperfusion injury and its related anti-inflammatory mechanism. Method 1: 1. 70 SD rats were randomly divided into 7 groups: model group, sham operation group, preconditioning group, Wenxindan 1:1:1 group, Wanxindan 1:2:1 group, Wanxindan 1:1:2 group and Wenxindan 1:1:2 group. The effect of CK-MBN cTnI on serum and myocardial infarction area in model rats was detected, and the optimal compatibility ratio group was selected by quantitative examination of compatibility ratio of Wanxin Dan. The effects of Wenxindan on the ultrafine structure of myocardium in rats with myocardial ischemia-reperfusion injury were observed by transmission electron microscope, and the expression of T-AktP- Akt in myocardial tissue was detected by immunohistochemical method. So as to explore the mechanism of Wenxin Dan on myocardial ischemia reperfusion injury. 3. The effects of Wenxindan on the protein distribution and expression of NF- 魏 B, COX-2 in myocardial tissue of rats with myocardial ischemia-reperfusion injury were detected by Western blot and immunohistochemistry. To observe the effect of Wenxindan on the content of TNF- 偽, IL-1 尾 and IL-6IL-10 in serum of myocardial ischemia-reperfusion injury model rats, and to explore its anti-inflammatory mechanism. The result is 1: 1. The serum CK-MBN cTnI content in rats with myocardial ischemia-reperfusion injury was significantly decreased in each treatment group, and the myocardial infarction area was decreased in MIRI model rats, among which the effect of Wanxindan 1:2:1 group was the most significant. 2. Compared with the model group, Wenxindan 1:2:1 group could significantly improve the myocardial ultrafine structure and increase the expression of p-Akt protein. 3. Compared with model group, Wenxindan 1:2:1 group could significantly inhibit the distribution and expression of COX-2 protein in myocardial tissue of myocardial ischemia-reperfusion injury model rats. Compared with the model group, Wenxindan 1:2:1 group could significantly reduce the content of TNF- 偽, IL-1 尾, IL-6 and increase the content of IL-10 in the serum of myocardial ischemia-reperfusion injury model rats. Conclusion 1. The content of myocardial enzyme CK-MBN cTnI in rats with myocardial ischemia-reperfusion injury was significantly decreased in the groups of different combinations of Wenxindan, and the myocardial infarction area of MIRI model rats was reduced. The best proportion of anti-myocardial ischemia and reperfusion was chosen as the 1:2:1 group of Wenxindan group. 2. Through activating PI3K / Akt signal transduction pathway, Wanxin Dan can increase the expression of p-Akt protein, decrease the expression of NF- 魏 B, decrease the degree of myocardial injury, and play a protective role in myocardium. Through activating PI3K / Akt signal transduction pathway, Wanxin Dan can down-regulate the expression of inflammatory factor TNF- 偽, IL-1 尾 and IL-6, promote the release of anti-inflammatory factor IL-10, and then play a protective role in myocardium.
【學(xué)位授予單位】：黑龍江中醫(yī)藥大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R285.5;R-332

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1 沈曉璞;穩(wěn)心丹不同比例配伍對(duì)MIRI模型大鼠抗炎機(jī)制研究[D];黑龍江中醫(yī)藥大學(xué);2017年

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本文編號(hào)：2110962