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A Rapamycin-Enhanced Autophagy Reduces Neural Apoptosis by Blocking Bax Mitochondral Translation and Cytochrome C Release in Acute Spinal Cord Injury in Rats

Spinal cord injury (SCI) is a severe central nerve system damage. The actual roles of autophagy in the context of SCI remain controversial. This study was undertaken to determine the effects of enhanced autophagy on neural apoptosis in rat SCI model. Rapamycin or vehicle was given via an intraperitoneal injection after SCI. Spinal cord samples were extracted 24 hr after SCI. The level of phosphorylation of p70S6K was significantly reduced whereas expression of LC3-II/LC3-I was significantly increased after rapamycin treatment. Rapamycin treatment markedly reduced caspase-3 activity and staining density of TUNEL, but increased NeuN expression within the injured spinal cord. Moreover, rapamycin treatment reduced Bax translocation to the mitochondria and the release of cytochrome c into the cytosol. Rapamycin-treated rats showed significantly higher locomotor function in BBB scores compared with vehicletreated rats. Our results demonstrated rapamycinenhanced autophagy reduced neuronal apoptosis via inhibiting mTOR signal pathway, and improved locomotory recovery in rat SCI model. The antiapoptotic mechanism was related to the enhancement of autophagy, which ameliorated neural apoptosis through a mitochondrial pathway.


Junhua Du, Xigong Li, Xiangjin Lin, Yang Lu and Bin Chen

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