Effects of Glutathione on Mechanical Allodynia and Central Sensitization in Chronic Postischemic Pain Rats.

Jinseok Yeo,Hyerim Lee,Hoon Jung

doi:10.1155/2017/7394626

Abstract

Background The chronic postischemia pain (CPIP) model is an animal model using ischemia/reperfusion injury that mimics the symptoms of complex regional pain syndrome type I. Glutathione (GSH) prevents ischemia/reperfusion injury by scavenging free radicals. We conducted this study to investigate the protective effect of GSH in CPIP rats via changes of mechanical allodynia and phospholyration of the N-methyl-D-aspartate receptor subunit GluN1. Methods We divided 45 rats into 5 groups: sham, CPIP, CPIP + GSH 100 mg/kg, CPIP + GSH 200 mg/kg, and CPIP + GSH 500 mg/kg. Rats in the sham and CPIP groups received normal saline and rats in the other groups received GSH at the designated doses thirty minutes prior to reperfusion. Withdrawal thresholds were evaluated before sugery as well as 1, 3, and 7 days after surgery. pGluN1 level in the spinal cord was also measured. Results GSH treated rats show a significant increase in the withdrawal thresholds of both hind paws as compared with the CPIP group dose-dependently. The expression of pGluN1 in the GSH treated rats significantly decreased as compared to the CPIP group (all P < 0.05). Conclusion These findings suggest that GSH inhibited the development of mechanical allodynia and central sensitization in CPIP rats.

Highlights

Complex regional pain syndrome type I (CRPS I) is a devastating condition that usually affects a limb and is not accompanied by a clinically verifiable nerve injury [1]
We hypothesized that the protective effect of GSH on ONOO− associated injury could attenuate the development of mechanical allodynia and central sensitization in chronic postischemia pain (CPIP) rats that mimics the symptoms of human CRPS I
Our study has showed that the treatment with GSH prior to reperfusion attenuated mechanical allodynia and suppressed spinal phosphorylation of GluN1 in CPIP rats dosedependently

Summary

Background

The chronic postischemia pain (CPIP) model is an animal model using ischemia/reperfusion injury that mimics the symptoms of complex regional pain syndrome type I. Glutathione (GSH) prevents ischemia/reperfusion injury by scavenging free radicals. We divided 45 rats into 5 groups: sham, CPIP, CPIP + GSH 100 mg/kg, CPIP + GSH 200 mg/kg, and CPIP + GSH 500 mg/kg. Rats in the sham and CPIP groups received normal saline and rats in the other groups received GSH at the designated doses thirty minutes prior to reperfusion. GSH treated rats show a significant increase in the withdrawal thresholds of both hind paws as compared with the CPIP group dose-dependently. The expression of pGluN1 in the GSH treated rats significantly decreased as compared to the CPIP group (all P < 0.05). These findings suggest that GSH inhibited the development of mechanical allodynia and central sensitization in CPIP rats

Introduction

45 Sprague-Dawley rats

Materials and Methods

Results

Discussion

Conflicts of Interest