• Jinseok Yeo, Hoon Jung, and Hyerim Lee.
• Department of Anesthesiology and Pain Medicine, Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
• Pain Res Manag. 2017 Jan 1; 2017: 7394626.

BackgroundThe 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.MethodsWe 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.ResultsGSH 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).ConclusionThese findings suggest that GSH inhibited the development of mechanical allodynia and central sensitization in CPIP rats.

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