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Neural Regen Res. 2016 Jun;11(6):977-82. doi: 10.4103/1673-5374.184498.

Atorvastatin activates autophagy and promotes neurological function recovery after spinal cord injury.

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Department of Physiology, Jinzhou Medical University, Jinzhou, Liaoning Province, China.
Department of Orthopedics, Jinzhou Municipal Second Hospital, Jinzhou, Liaoning Province, China.
Department of Orthopedics, Jining No. 1 People's Hospital, Jining, Shandong Province, China.
Jinzhou Central Hospital, Jinzhou, Liaoning Province, China.
Department of Orthopedics, Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, China.
Department of Orthopedics, First Hospital of Qinhuangdao City, Qinhuangdao, Hebei Province, China.


Atorvastatin, a lipid-lowering medication, provides neuroprotective effects, although the precise mechanisms of action remain unclear. Our previous studies confirmed activated autophagy following spinal cord injury, which was conducive to recovery of neurological functions. We hypothesized that atorvastatin could also activate autophagy after spinal cord injury, and subsequently improve recovery of neurological functions. A rat model of spinal cord injury was established based on the Allen method. Atorvastatin (5 mg/kg) was intraperitoneally injected at 1 and 2 days after spinal cord injury. At 7 days post-injury, western blot assay, reverse transcription-polymerase chain reaction, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining results showed increased Beclin-1 and light chain 3B gene and protein expressions in the spinal cord injury + atorvastatin group. Additionally, caspase-9 and caspase-3 expression was decreased, and the number of TUNEL-positive cells was reduced. Compared with the spinal cord injury + saline group, Basso, Beattie, and Bresnahan locomotor rating scale scores significantly increased in the spinal cord injury + atorvastatin group at 14-42 days post-injury. These findings suggest that atorvastatin activated autophagy after spinal cord injury, inhibited apoptosis, and promoted recovery of neurological function.


Beclin-1; apoptosis; atorvastatin; autophagy; light chain 3B; motor function recovery; nerve regeneration; neural regeneration; neuroprotection; secondary injury; spinal cord injury; statins

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