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
【24h】

Activation of autophagy in rat brain cells following focal cerebral ischemia reperfusion through enhanced expression of Atg1/pULK and LC3

机译:通过增强Atg1 / pULK和LC3的表达激活局灶性脑缺血再灌注后大鼠脑细胞自噬的激活

获取原文
获取原文并翻译 | 示例
       

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:本研究旨在研究局灶性脑缺血再灌注(CIR)损伤后大脑皮层中Atg1 / pULK和LC3的活化,从而研究其对脑细胞自噬的影响。使用大脑中动脉闭塞技术建立大鼠CIR模型。用神经功能评分,TTC染色和脑组织含水量评估CIR模型。使用电子显微镜检查CIR损伤后不同时间点的脑细胞自噬水平。免疫组织化学和蛋白质印迹分析还用于定性和定量检测大脑皮层中Atg1 / pULK和LC3的水平。 CIR早期观察到自噬,CIR后1 h观察到Atg1 / pULK和LC3的表达,并在12 h后达到峰值表达水平,此后逐渐下降。这些结果表明Atg1 / pULK和LC3是大鼠脑CIR后自噬调节的关键。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号