N-acetylcysteine downregulates phosphorylated p-38 expression but does not reverse the increased superoxide anion levels in the spinal cord of rats with neuropathic pain

Brazilian Journal of Medical and Biological Research, 2017 · DOI: 10.1590/1414-431X20165801 · Published: January 1, 2017

Spinal Cord Injury Pharmacology Pain Management

Simple Explanation

This study investigates how N-acetylcysteine (NAC) affects phosphorylated p38 protein expression and superoxide anion generation in rats with neuropathic pain. The sciatic functional index (SFI) was measured to assess functional recovery after nerve lesion. The study found that NAC reduced p-p38 expression but did not reverse increased superoxide anion generation.

Study Duration

7 days

Participants

36 male Wistar rats

Evidence Level

Not specified

Key Findings

1
CCI induced a decrease in SFI as well as an increase in p-p38 expression and SAG in the spinal cord.
2
NAC induced a downregulation in p-p38 expression at all time-points evaluated, but did not reverse the increased SAG induced by CCI.
3
The recovery was 44% in NAC-treated CCI rats, compared to values from CCI rats at day 1.

Research Summary

The study examined the effect of NAC on p-p38 expression and superoxide anion generation (SAG) in the spinal cord of rats with CCI-induced neuropathic pain. CCI led to decreased SFI and increased p-p38 expression and SAG. NAC treatment improved SFI recovery and reduced p-p38 expression but did not affect SAG. The findings suggest that modulation of p-p38 by NAC may play a role in its effects on neuropathic pain and nerve regeneration.

Practical Implications

Therapeutic Potential

NAC may be a potential therapeutic agent for managing neuropathic pain through modulation of p-p38 expression.

Further Research

Further studies are needed to clarify the relationship between NAC, p-38, and nitric oxide in the spinal cord of CCI rats.

Functional Nerve Recovery

NAC treatment attenuates ongoing spontaneous pain, and leads to better functional recovery after nerve injury.

Study Limitations

1
The study did not elucidate the mechanism by which NAC modulates p-p38 expression.
2
The inability of NAC to reverse increased SAG levels limits its potential as a complete solution for neuropathic pain.
3
The study only used male Wistar rats, which may limit the generalizability of the findings to other populations.

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