【摘要】：目的:研究舒芬太尼后處理對(duì)非糖尿病(non-diabetic mellitus,NDM)和糖尿病大鼠(diabetic mellitus,DM)心肌缺血再灌注損傷(Myocardial ischemia/reperfusion injury,MI/RI)的影響及其與磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)-蛋白激酶B(Akt)通路、細(xì)胞色素C(Cytochrome C,Cyt-C)的關(guān)系。方法:選擇健康SD大鼠二十四只,利用隨機(jī)數(shù)字表法,將其分為四組(n=6):分別是NDM假手術(shù)組(NDM-S組)、缺血再灌注組(NDM-I/R組)、舒芬太尼后處理組(NDM-SP組)、舒芬太尼后處理+渥曼青霉素(PI3K抑制劑)組(NDM-SP+W組)。另外重新選擇健康SD大鼠,將其制備成DM大鼠,選取造模成功的大鼠二十四只,將其也分為四組(n=6):DM假手術(shù)組(DM-S組)、缺血再灌注組(DM-I/R組)、舒芬太尼后處理組(DM-SP組)、舒芬太尼后處理+渥曼青霉素組(DM-SP+W組)。結(jié)扎其LAD制備大鼠MI/RI的模型。其中S組只穿線(xiàn)不結(jié)扎;I/R組穿線(xiàn)后穩(wěn)定5min,阻斷30min,再灌注120min;SP組于恢復(fù)灌注前5min靜注舒芬太尼1.0μg/kg;SP+W組于恢復(fù)灌注前5min靜注渥曼青霉素15μg/kg和舒芬太尼1.0μg/kg。實(shí)驗(yàn)完畢后取血,測(cè)肌鈣蛋白I(c Tn I)的濃度;處死大鼠并收集心肌組織,采用TUNEL法測(cè)定心肌細(xì)胞的凋亡指數(shù)(AI);Western blot法檢測(cè)心肌組織Akt、p-Akt、Cyt-C的表達(dá)水平。結(jié)果:舒芬太尼后處理可明顯減輕NDM組的MI/RI,使升高的c Tn I濃度降低、AI降低,p-Akt的表達(dá)增加、Cyt-C的表達(dá)下調(diào),而對(duì)DM組MI/RI的各項(xiàng)指標(biāo)均無(wú)明顯的影響。NDM-SP組的血漿c Tn I的濃度、AI、Cyt-C的表達(dá)明顯低于DM-SP組而p-Akt的表達(dá)高于DM-SP組。結(jié)論:舒芬太尼后處理對(duì)NDM大鼠MI/RI有保護(hù)作用,通過(guò)PI3K-Akt通路減少了Cyt-C的釋放。而對(duì)DM大鼠MI/RI沒(méi)有保護(hù)作用,PI3K-Akt通路不參與該過(guò)程。
[Abstract]:Aim: to study the effects of sufentanil postconditioning on myocardial ischemia-reperfusion injury (Myocardial ischemia/reperfusion / RI) in non-diabetic Mellitus diabetic rats and its relationship with phosphatidylinositol 3-kinase- PI3K-protein kinase B (Akt) pathway, cytochrome C (Cytochrome Cyt-C. Methods: 24 healthy Sprague-Dawley rats were selected. They were divided into four groups: NDM sham-operation group (NDM-S group), ischemia-reperfusion group (NDM-I/R group), sufentanil post-treatment group (NDM-SP group) and sufentanil post-treated womanpenicillin (NDM-SP W group). In addition, healthy SD rats were re-selected and made into DM rats. 24 rats were selected for successful modeling. They were also divided into four groups: sham operation group (DM-S group), ischemia reperfusion group (DM-I/R group), sufentanil aftertreatment group (DM-SP group), and sufentanil aftertreatment group (DM-SP W group). The rat model of MI/RI was established by ligating its LAD. In S group, sufentanil 1.0 渭 g / kg SP W was injected intravenously with womanpenicillin 15 渭 g/kg and sufentanil 1.0 渭 g / kg 路kg before reperfusion in group S, only 5 minutes after ligation without ligation, and 30 minutes after occlusion, and 120 minutes after reperfusion. The patients in group S received intravenous injection of sufentanil (1.0 渭 g / kg) and sufentanil (15 渭 g / kg) before reperfusion. At the end of the experiment, the concentration of troponin I (c Tn I) was measured, and the myocardial tissue was collected and killed. The apoptosis index (AI) of myocardial cells was measured by TUNEL, and the expression of Akttip-Akttiocyt C in myocardial tissue was detected by (AI) blot. Results: after treatment with sufentanil, MI-RI in NDM group was significantly alleviated, and the increased c Tn I concentration decreased the expression of p-Akt, increased the down-regulation of Cyt-C expression. However, there was no significant effect on the indexes of MI/RI in DM group. The level of plasma c Tn I in NDM-SP group was significantly lower than that in DM-SP group, and the expression of p-Akt was higher than that in DM-SP group. Conclusion: sufentanil post-treatment has protective effect on MI/RI in NDM rats and reduces the release of Cyt-C through PI3K-Akt pathway. The PI3 K-Akt pathway was not involved in the process of MI/RI in DM rats.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類(lèi)號(hào)】：R614

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