本文選題：氧-葡萄糖剝奪 + 心肌細(xì)胞　； 參考：《南京醫(yī)科大學(xué)》2016年博士論文

【摘要】：研究目標(biāo)：哌立福新是一種Akt抑制劑,令人驚訝的是我們發(fā)現(xiàn)低濃度哌立福新具有保護(hù)心肌免受氧葡萄糖剝奪(OGD)/再氧合作用,本項(xiàng)目的實(shí)驗(yàn)?zāi)康氖沁M(jìn)一步探索哌立福新對心肌細(xì)胞缺血再灌注損傷的保護(hù)作用及該保護(hù)作用的可能機(jī)制。實(shí)驗(yàn)方法和結(jié)果：1.檢測不同濃度的派立福辛對H9c2細(xì)胞存活的影響,并檢測經(jīng)低濃度(0.1-0.5μM)哌立福新處理后不同作用時(shí)間H9c2細(xì)胞的活力,發(fā)現(xiàn)低濃度派立福辛對心肌細(xì)胞有保護(hù)作用,而且低濃度哌立福新可以保護(hù)H9c2細(xì)胞受到的氧糖剝奪/再氧合損傷。2.檢測低濃度派立(0.1-0.5μM)福辛對氧糖剝奪誘導(dǎo)活性氧、線粒體Cyp-D-p53結(jié)合物及線粒體膜電位(MMP)的影響,表明低濃度派立福辛可抑制糖剝奪/再氧合引起的氧化應(yīng)激反應(yīng)。3.檢測AMPK信號通路在低濃度哌立福新(0.1-0.5μM)保護(hù)心肌細(xì)胞中的作用,并通過構(gòu)建慢病毒shRNA轉(zhuǎn)染H9c2細(xì)胞及對新生小鼠心肌細(xì)胞使用AMPKal siRNA敲除基因來抑制AMPK,發(fā)現(xiàn)哌立福新介導(dǎo)的抗氧化與細(xì)胞保護(hù)作用被大大減弱。實(shí)驗(yàn)結(jié)論：低濃度哌立福新(0.1-0.5 gM)在H9c2細(xì)胞受到的氧糖剝奪／再氧合發(fā)生損傷時(shí)起保護(hù)作用。其機(jī)制可能與低濃度派立福辛能通過誘導(dǎo)AMPK信號通路激活,對抗氧糖剝奪／再氧合介導(dǎo)抗氧化有關(guān)。本研究提示低濃度的哌立福新有可能成為臨床上治療心肌缺血再灌注損傷的一種新的方法。
[Abstract]:Objective: piperidoxin is a Akt inhibitor, and surprisingly, we found that low concentrations of pirifoxacin can protect myocardium from oxygen and glucose deprivation and can be used in combination with OGDX / reoxygenation. The aim of this study was to explore the protective effect of pirifoxacin on myocardial ischemia-reperfusion injury and its possible mechanism. Experimental methods and results: 1. The effects of different concentrations of pirifampicin on the survival of H9c2 cells were detected, and the viability of H9c2 cells treated with low concentration of pirifoxacin 0.1-0.5 渭 m for different time was detected. It was found that low concentration of pirifampicin had protective effect on cardiomyocytes. And the low concentration of piperfon can protect H9c2 cells from oxygen glucose deprivation / reoxygenation injury. 2. The effects of low concentration of piridol 0.1-0.5 渭 M) on oxygen glucose deprivation induced reactive oxygen species (Ros), mitochondrial Cyp-D-p53 conjugates and mitochondrial membrane potentials (mMPs) were determined, indicating that low concentration of pirifampicin could inhibit oxidative stress induced by glucose deprivation / reoxygenation. The role of AMPK signaling pathway in the protection of cardiomyocytes from 0. 1-0. 5 渭 M of piprafon at low concentration was detected. By constructing lentivirus shRNA to transfect H9c2 cells and using AMPKal siRNA knockout gene to inhibit AMPK in neonatal mouse cardiomyocytes, it was found that the antioxidation and cell protection mediated by piperidoxin were greatly weakened. Conclusion: the low concentration of pirifampicin 0.1-0.5 g M may protect H9c2 cells from oxygen glucose deprivation / reoxygenation injury. The mechanism may be related to the low concentration of parifoxine by inducing activation of AMPK signaling pathway, and antagonizing oxygen glucose deprivation / reoxygenation mediated oxidation. This study suggests that low-concentration piperidoxacin may be a new method for the treatment of myocardial ischemia-reperfusion injury.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R542.2

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