本文選題：NECA + 心肌缺血再灌注損傷�。� 參考：《醫(yī)學(xué)研究生學(xué)報(bào)》2017年06期

【摘要】：目的腺苷受體激動(dòng)劑NECA具有一定的心肌保護(hù)作用,但具體機(jī)制尚不明確。文中探討NECA對(duì)大鼠心肌缺血再灌注損傷內(nèi)質(zhì)網(wǎng)應(yīng)激的作用及機(jī)制。方法選取SPF級(jí)雄性成年Wistar大鼠56只,利用Langendorff裝置制成大鼠離體心臟缺血再灌注損傷模型。隨機(jī)數(shù)字表法分為假手術(shù)組、缺血再灌注組、腺苷受體激動(dòng)劑組和內(nèi)質(zhì)網(wǎng)應(yīng)激抑制劑組,每組14只。假手術(shù)組:心臟穿線但不結(jié)扎,用Kerbs-Henseleit緩沖液持續(xù)灌流170 min;缺血再灌注組:心臟穩(wěn)定20 min,缺血30min,再灌注2 h;腺苷受體激動(dòng)劑組、內(nèi)質(zhì)網(wǎng)應(yīng)激組:心臟穩(wěn)定20 min,缺血30 min,再灌注2 h,于再灌注前5 min分別給予含0.1μmol/L NECA的灌流液、30μmol/L TUDCA的灌流液,均至再灌注30 min時(shí)結(jié)束。透射電鏡觀察心肌超微結(jié)構(gòu)的變化;Western blot方法檢測(cè)內(nèi)質(zhì)網(wǎng)應(yīng)激IREl-XBPl信號(hào)通路標(biāo)志蛋白IRE1α、XBP1s的表達(dá)水平;免疫組化觀察IRE1α的表達(dá)情況。結(jié)果透射電鏡結(jié)果顯示,缺血再灌注組大部分肌絲斷裂,肌節(jié)攣縮變形,可見線粒體空泡變性;腺苷受體激動(dòng)劑組及內(nèi)質(zhì)網(wǎng)應(yīng)激組較缺血再灌注組損傷減輕,表現(xiàn)為肌絲排列較整齊,肌節(jié)僅有輕度攣縮。免疫組化結(jié)果發(fā)現(xiàn),假手術(shù)組基本無(wú)IRE1α陽(yáng)性染色,缺血再灌注組IRE1α陽(yáng)性染色區(qū)域顯著增加,而NECA和內(nèi)質(zhì)網(wǎng)應(yīng)激抑制劑組IRE1α陽(yáng)性染色部位明顯減少。與假手術(shù)組相比,缺血再灌注組的IRE1α和XBP1s蛋白的表達(dá)水平明顯上升(P0.05);而與缺血再灌注組IRE1α和XBP1s的蛋白表達(dá)水平(1.72±0.27、0.97±0.19)相比,腺苷受體激動(dòng)劑組(1.14±0.16、0.60±0.13)及內(nèi)質(zhì)網(wǎng)應(yīng)激抑制劑組(1.07±0.27、0.58±0.15)顯著降低(P0.05)。結(jié)論 NECA可通過抑制IREl-XBPl信號(hào)通路來(lái)減輕內(nèi)質(zhì)網(wǎng)應(yīng)激,從而發(fā)揮心肌保護(hù)作用。
[Abstract]:Objective adenosine receptor agonist (NECA) has a protective effect on myocardium, but the mechanism is unclear. To investigate the effect and mechanism of NECA on endoplasmic reticulum stress during myocardial ischemia reperfusion injury in rats. Methods Fifty-six adult SPF male Wistar rats were selected and the model of isolated heart ischemia-reperfusion injury was established by Langendorff device. The rats were randomly divided into sham-operated group, ischemia-reperfusion group, adenosine receptor agonist group and endoplasmic reticulum stress inhibitor group with 14 rats in each group. Sham operation group: the heart pierced but not ligated, perfused continuously with Kerbs-Henseleit buffer for 170min; Ischemia-reperfusion group: cardiac stability 20 min, ischemia 30 min, reperfusion 2 h; adenosine receptor agonist group, adenosine receptor agonist group, In the endoplasmic reticulum stress group, the heart was stable for 20 minutes, ischemia for 30 minutes, reperfusion for 2 hours, and perfused with 0.1 渭 mol/L NECA of 30 渭 mol/L TUDCA at 5 min before reperfusion until 30 min after reperfusion. The changes of myocardial ultrastructure were observed by transmission electron microscope. The expression of IRE1 偽 XBP1s, a marker of IREl-XBPl signaling pathway in endoplasmic reticulum stress, and the expression of IRE1 偽 were detected by Western blot. Results the results of transmission electron microscope showed that most of the myofilms were broken and the sarcomere contracture was deformed in the ischemia-reperfusion group, the vacuolar degeneration of mitochondria was observed, the damage of adenosine receptor agonist group and endoplasmic reticulum stress group was less than that of the ischemia reperfusion group. The myofilaments were arranged neatly, and the sarcomere was only slightly contracture. The immunohistochemical results showed that there was no IRE1 偽 positive staining in sham-operated group, but the area of IRE1 偽 positive staining in ischemia-reperfusion group was significantly increased, while that in NECA and endoplasmic reticulum stress inhibitor group was significantly decreased. Compared with sham operation group, the expression level of IRE1 偽 and XBP1s protein in ischemia reperfusion group was significantly higher than that in ischemia reperfusion group, but the protein expression level of IRE1 偽 and XBP1s in ischemia reperfusion group was 1.72 鹵0.270.97 鹵0.19), the expression level of IRE1 偽 and XBP1s in adenosine receptor agonist group was 1.14 鹵0.160.60 鹵0.13) and that in endoplasmic reticulum stress inhibitor group (1.07 鹵0.270.58 鹵0.15) was significantly lower than that in ischemia-reperfusion group (1.72 鹵0.270.97 鹵0.19), and that in endoplasmic reticulum stress inhibitor group (1.07 鹵0.270.58 鹵0.15) was significantly lower than that in sham operation group. Conclusion NECA can attenuate endoplasmic reticulum stress by inhibiting IREl-XBPl signaling pathway, thus exerting myocardial protection.
【作者單位】： 華北理工大學(xué)護(hù)理與康復(fù)學(xué)院;
【基金】：河北省人才工程培養(yǎng)經(jīng)費(fèi)資助[冀人社字(2012)334] 河北省科技廳基金項(xiàng)目(16277787D)
【分類號(hào)】：R54

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