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首页> 外文期刊>Molecular medicine reports >Activation of autophagy in rat brain cells following focal cerebral ischemia reperfusion through enhanced expression of Atg1/pULK and LC3
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Activation of autophagy in rat brain cells following focal cerebral ischemia reperfusion through enhanced expression of Atg1/pULK and LC3

机译:局灶性脑缺血再灌注后大鼠脑细胞的激活通过增强ATG1 /折叠和LC3

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摘要

The present study aimed to investigate the activation of Atg1/pULK, and LC3 in the cerebral cortex following focal cerebral ischemia reperfusion (CIR) injury, thereby examining its effect on autophagy in brain cells. Rat CIR models were established using the technique of middle cerebral artery occlusion. The neurological function score, TTC staining and the water content of brain tissue were used to evaluate the CIR model. Levels of autophagy in the brain cells were examined at different time-points following CIR damage using electron microscopy. Immunohistochemistry and western blot analysis were also used for the qualitative and quantitative detection of levels of Atg1/pULK and LC3 in the cerebral cortex. Autophagy was observed in the early stage of CIR, and the expression of Atg1/pULK and LC3 were observed 1 h following CIR in the rats and reached peak expression levels after12 h, which following which the they gradually decreased. These results suggested Atg1/pULK and LC3 are key in the regulation of autophagy following CIR in the rat brain.
机译:本研究旨在探讨局灶性脑缺血再灌注(CIR)损伤后脑皮质中的ATG1 /乳膏和LC3的活化,从而检查其对脑细胞中自噬的影响。使用中间脑动脉闭塞技术建立了大鼠CIR模型。使用神经功能评分,TTC染色和脑组织的含水量来评估CIR模型。使用电子显微镜损伤后的不同时间点检查脑细胞中的自噬水平。免疫组织化学和Western印迹分析也用于脑皮质中的ATG1 /乳膏和LC3水平的定性和定量检测。在CIR的早期观察到自噬,并观察到大鼠中的1小时内的ATG1 /ρ和LC3的表达,并且在12小时后达到峰表达水平,它们逐渐降低。这些结果表明ATG1 /乳膏和LC3是大鼠脑中自噬调节的关键。

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