Neuroprotective effects of rapamycin on spinal cord injury in rats by increasing autophagy and Akt signaling

Neural Regeneration Research, 2019 · DOI: 10.4103/1673-5374.247476 · Published: April 1, 2019

Simple Explanation

This study investigates the neuroprotective effects of rapamycin on spinal cord injury (SCI) in rats. Rapamycin is known to enhance autophagy and activate Akt signaling, both of which can protect cells from damage. The researchers used a rat model of SCI to test whether rapamycin could reduce nerve damage by increasing autophagy and activating Akt phosphorylation. They also used inhibitors to block autophagy and Akt signaling to see if they would reduce the protective effects of rapamycin. The results showed that rapamycin reduced the expression of molecules related to apoptosis (cell death) in the injured spinal cord tissue. Inhibiting autophagy and Akt signaling reduced the protective effect of rapamycin on apoptotic neurons. Thus, rapamycin protects against SCI by activating autophagy and the Akt signaling pathway.

Study Duration

Not specified

Participants

72 adult male Sprague-Dawley rats

Evidence Level

Level 3; Animal study

Key Findings

1
Rapamycin inhibits mTOR expression and up-regulates Beclin 1 and phosphorylated-Akt expression in injured spinal cord tissue.
2
Rapamycin prevents the decrease of Bcl-2 expression and reduces Bax, cytochrome c, and caspase-3 expression in injured spinal cord tissue, thereby reducing apoptotic neurons.
3
Inhibition of autophagy and Akt signaling pathways attenuates the neuroprotective effects of rapamycin on apoptotic neurons after spinal cord injury.

Research Summary

This study aimed to investigate the neuroprotective effects of rapamycin on spinal cord injury (SCI) in rats by examining its impact on autophagy and Akt signaling pathways. The results demonstrated that rapamycin treatment inhibited mTOR, upregulated Beclin 1 and phosphorylated-Akt, prevented the decrease of Bcl-2, and reduced Bax, cytochrome c, and caspase-3 expression, leading to a reduction in apoptotic neurons. Furthermore, the study found that inhibiting autophagy and Akt signaling attenuated the protective effects of rapamycin on neural apoptosis, indicating that both pathways play crucial roles in the neuroprotective mechanism of rapamycin.

Practical Implications

Therapeutic Potential

Rapamycin may be a potential therapeutic agent for treating spinal cord injury by promoting autophagy and activating Akt signaling.

Pathway Targeting

Targeting both autophagy and Akt signaling pathways could be a promising strategy for neuroprotection in SCI.

Combination Therapy

Combining rapamycin with other neuroprotective agents may enhance the therapeutic efficacy in SCI treatment.

Study Limitations

1
The study was conducted on a rat model, and the results may not be directly applicable to humans.
2
The study only examined the effects of rapamycin at a single time point (24 hours after SCI), and the long-term effects are unknown.
3
The specific mechanisms by which rapamycin activates autophagy and Akt signaling in SCI were not fully elucidated.

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