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Changes in autophagy after traumatic brain injury

    Autophagy is the chief machinery for bulk degradation of superfluous or aberrant cytoplasmic components. This study used the rat moderate fluid percussion injury model to investigate whether the autophagy pathway plays a key role after traumatic brain injury (TBI). Induction of autophagy is manifested by accumulation of autophagosomes (APs), observable under transmission electron microscopy (EM). Two hallmarks of autophagy, i.e., the microtubule-associated protein light chain 3 (LC3)-II and the autophagy-related gene (ATG)12-ATG5 conjugates, were explored by biochemical and confocal microscopic analyses of brain tissues. Under EM, both APs and autolysosomes were markedly accumulated in neurons from 4 h onward after TBI. Western blot analysis showed that ATG12-ATG5 conjugate was markedly redistributed during 5 to 15 days in brain tissues after TBI. LC3-II conjugate was initially unchanged but was drastically upregulated from 24 h onward in the pre-AP-containing fraction after TBI. LC-3 immunostaining was mainly located in living neurons under confocal microscopy. These results clearly show that the autophagy pathway is persistently activated after TBI. Because the autophagy pathway is the chief machinery for bulk elimination of aberrant cell components, we propose that activation of this pathway serves as a protective mechanism for maintaining cellular homeostasis after TBI.

外伤性脑损伤后的自噬变化

   自噬是一种大量降解细胞质内过剩或异常成分的主要机制。本研究采用适度液体撞击所诱导的大鼠脑损伤模型，探究在外伤性脑损伤后自噬途径是否起了关键性作用。自噬小体（APs）的积聚代表了自噬的诱导，该现象可以通过透射电镜进行观察。对脑组织进行生化检测和共焦显微镜观察可以探查自噬的两个标记物：微管相关蛋白轻链3（LC3-Ⅱ）以及自噬相关基因ATG12-ATG5结合物。电镜观察发现：自噬小体(APS)和自噬溶酶体(ALS)在外伤性脑损伤（TBI）后4h在神经元内显著地积聚。蛋白印记分析在TBI后5天到15天，脑组织内ATG12-ATG5结合物重新分布显著。LC3-Ⅱ结合物最初没有改变，但是在TBI后24h开始，在前自噬小体包含成分内大幅上调。共聚焦显微镜观察LC3免疫染色主要位于存活着神经细胞元内。这些结果清楚地显示：在TBI后自噬途径持续地活化。由于自噬途径是大量清除异常细胞成分的主要机制，我们推测：在TBI后自噬途径的活化作为维持细胞稳态的保护性机制。