Water Treadmill Training Ameliorates Neurite Outgrowth Inhibition Associated with NGR/RhoA/ROCK by Inhibiting Astrocyte Activation following Spinal Cord Injury

Oxidative Medicine and Cellular Longevity, 2022 · DOI: https://doi.org/10.1155/2022/1724362 · Published: March 27, 2022

Spinal Cord Injury Neurology Rehabilitation

Simple Explanation

Spinal cord injury (SCI) often results in damage to or degeneration of axons. Rehabilitative training is a recognized method for the treatment of SCI, but the speciﬁc mechanism underlying its eﬀect on axonal outgrowth in the central nervous system (CNS) has not yet been determined. This study combined a treadmill with swimming and used the water treadmill to explore the mechanism underlying neurite outgrowth after SCI. We found that TT played a novel role in recovery from SCI by promoting axonal outgrowth associated with NGR/RhoA/ROCK signaling by inhibiting astrocyte activation after SCI.

Study Duration

7 or 14 d

Participants

190 adult male SD rats

Evidence Level

Not specified

Key Findings

1
TT decreased tissue structure damage and improved functional recovery after SCI.
2
TT promoted the regeneration of neurons and reduced apoptosis around the lesion.
3
TT inhibited the injury-induced increase in the expression of proinﬂammatory factors.

Research Summary

This study investigates the effect of water treadmill training (TT) on neurite outgrowth after spinal cord injury (SCI) in rats. The results showed that TT decreased tissue damage, improved functional recovery, promoted neuron regeneration, and reduced apoptosis. TT also inhibited astrocyte and microglia activation, reduced pro-inflammatory factors, and modulated the NGR/RhoA/ROCK signaling pathway, suggesting a novel role in SCI recovery.

Practical Implications

Rehabilitation Strategy

Water treadmill training can be used as a non-drug means to reduce the inhibition of axonal growth in SCI rats and promote the recovery of nerve function.

Therapeutic Target

Targeting the transformation of A1- and A2-reactive astrocytes may be a strategy for the prevention and treatment of SCI.

Underlying Mechanism

TT can effectively promote axonal growth after SCI, partly by regulating RA activation to reduce activation of the RhoA/ROCK signaling pathway in neurons.

Study Limitations

1
Only male rats were included, ignoring possible sex differences in TT treatment.
2
The specific mechanisms underlying the effects of TT on astrocyte activation and the NGR/RhoA/ROCK pathway require further investigation.
3
The study does not address the long-term effects of TT on SCI recovery.

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