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KMID : 0356920130650050442
Korean Journal of Anesthesiology
2013 Volume.65 No. 5 p.442 ~ p.448
Antiallodynic effects of vitamin C and vitamin E in chronic post-ischemia pain rat model
Park Jun-Mo

Kim Chae-Kyung
Lee Hyung-Chul
Jung Hoon
Choi Kwang-Uk
Hong Seong-Wook
Lim Dong-Gun
Baek Woon-Yi
Kwak Kyung-Hwa
Abstract
Background: Recent research has shown that reactive oxygen species (ROS) play a significant role in the development and persistence of neuropathic pain through central sensitization via N-methyl-D-aspartate (NMDA) receptor activation. In the present study, we examined whether the intraperitoneal administration of vitamins C and E alone or together could alleviate mechanical allodynia in a chronic post-ischemia pain (CPIP) rat model.

Methods: Vitamins C and E were administered intraperitoneally to 48 male Sprague Dawley rats once per day for 3 days before hindpaw ischemia-reperfusion (I/R) injury was induced. On the third day, the CPIP rat model was produced by inducing ischemia in the left hindpaw by applying an O-ring for 3 h, followed by reperfusion. Three days after reperfusion, hindpaw mechanical allodynia was assessed by measuring the withdrawal response to von Frey filament stimulation. The rats were sacrificed immediately after behavioral testing to determine the phosphorylated NMDA receptor subunit 1 (pNR1) and extracellular-signal-regulated kinases (pERK) levels in the spinal cord.

Results: When the antioxidant vitamins C and E were administered intraperitoneally to CPIP rats, I/R injury-induced mechanical allodynia was attenuated, and pNR1 and pERK levels were decreased in the rat spinal cord. Additionally, the co-administration of both vitamins had an increased antiallodynic effect.

Conclusions: The reduced phosphorylated NR1 and ERK levels indicate that vitamins C and E inhibit the modulation of spinal cord neuropathic pain processing. Co-administration of vitamins C and E had a greater antiallodynic effect.
KEYWORD
Antioxidants, Complex regional pain syndromes, Mitogen-activated protein kinases, N-methyl-D-aspartate receptors, Reperfusion injury, Vitamins
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