本文選題：七氟醚后處理　切入點(diǎn)：心肌缺血再灌注損傷　出處：《山西醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:探討Mfn-2表達(dá)和PI3K-Akt通路在七氟醚后處理減輕大鼠心肌缺血再灌注損傷中的作用。方法:將30只雄性SD大鼠隨機(jī)分為五組(n=6):假手術(shù)(SH)組、心肌缺血再灌注損傷(MIRI)組、七氟醚后處理(SP)組、七氟醚+PI3K通道抑制劑Wortmannin(SP+W)組與Wortmannin(W)組。麻醉固定大鼠并暴露心臟,除外SH組,其余四組均結(jié)扎冠脈左前降支30min,復(fù)灌120min;SP組與SP+W組在復(fù)灌前10min吸入2.3%七氟醚15min;SP+W組在復(fù)灌前15min前經(jīng)股靜脈注射稀釋的渥曼青霉素(Wortmannin,15ug/kg);W組則只在復(fù)灌前15min靜注等量該抑制劑。全程記錄心電圖。結(jié)束后檢測指標(biāo):ELISA法測cTn-I;Western blot法檢測P-Akt(激活的Akt)、T-Akt(總Akt)并計(jì)算二者的比值,測Mfn-2的表達(dá);并在光鏡下觀察心肌細(xì)胞形態(tài)學(xué)的變化。結(jié)果:各組T-Akt表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05)。與SH組比較,余四組cTn-I含量表達(dá)上調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);與SP組比較,MIRI組、SP+W組以及W組的cTn-I表達(dá)上調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);MIRI組、SP+W組以及W組間的cTn-I含量表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05)。與SH組比較,余四組P-Akt表達(dá)上調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);與SP組比較,MIRI組、SP+W組以及W組的P-Akt表達(dá)下調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);MIRI組、SP+W組以及W組間的P-Akt表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05)。與SH組比較,余四組Mfn-2表達(dá)上調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);與SP組比較,MIRI組與W組的Mfn-2表達(dá)上調(diào),差異有統(tǒng)計(jì)學(xué)意義(P0.05);SP組與SP+W組的Mfn-2表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05),MIRI組與W組的Mfn-2表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05)。同時(shí),光鏡下細(xì)胞形態(tài)差異明顯,SH組無受損跡象,與SP組相比較,MIRI組、SP+W組以及W組受損更明顯。結(jié)論:1.七氟醚后處理減輕大鼠心肌缺血再灌注損傷可能與下調(diào)Mfn-2表達(dá)、激活PI3K-Akt通路有關(guān)。2.本實(shí)驗(yàn)七氟醚減輕MIRI的機(jī)制中,下調(diào)Mfn-2表達(dá)不在激活PI3K-Akt通路的下游。
[Abstract]:Aim: to investigate the role of Mfn-2 expression and PI3K-Akt pathway in reducing myocardial ischemia-reperfusion injury after sevoflurane treatment in rats.Methods: thirty male Sprague-Dawley rats were randomly divided into five groups: sham operation group, myocardial ischemia reperfusion injury group, sevoflurane post-treatment group, sevoflurane PI3K channel inhibitor Wortmannin(SP W group and Wortmanningnan group.Rats were anesthetized and exposed to heart, except SH group,The electrocardiogram was recorded.At the end of the study, the expression of Mfn-2 and the ratio of P-Akt (activated Akttium-Akt) were measured by the Western blot method, and the morphological changes of cardiomyocytes were observed under light microscope.Results: there was no significant difference in T-Akt expression in all groups (P 0.05).Compared with SH group, the expression of cTn-I was up-regulated in the other four groups, the difference was statistically significant (P 0.05), and the expression of cTn-I was up-regulated in SP-W and W groups compared with SP group.There was no significant difference in the expression of cTn-I between SP W group and W group.Compared with SH group, the expression of P-Akt in the other four groups was up-regulated, the difference was statistically significant (P 0.05), and the expression of P-Akt was down-regulated in SP W group and W group compared with SP group. There was no significant difference in P-Akt expression between SP W group and W group compared with SP group.Compared with SH group, the expression of Mfn-2 in the other four groups was up-regulated, the difference was statistically significant (P 0.05), and the expression of Mfn-2 was up-regulated in the other four groups compared with SP group and W group.There was no significant difference in Mfn-2 expression between SP group and SP W group. There was no significant difference in Mfn-2 expression between P0.05 and W group.At the same time, there was no significant difference in cell morphology under light microscope in SH group. Compared with SP group, the damage of MIRI group was more obvious than that of SP-W group and W group.Conclusion 1.The protective effect of sevoflurane on myocardial ischemia-reperfusion injury in rats may be related to down-regulation of Mfn-2 expression and activation of PI3K-Akt pathway.In this study, the down-regulation of Mfn-2 expression was not downstream of the activation of PI3K-Akt pathway in the mechanism of sevoflurane alleviating MIRI.
【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】：2017
【分類號(hào)】：R614

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