The effects of superoxide dismutase on the expression of c-fos gene in the chronic post-ischemic pain model rats. |
Tae Kyun Kim, Sang Wook Shin, Hoon Jung, Dong Gun Lim |
1Department of Anesthesiology and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea. 2Department of Anesthesiology and Pain Medicine, School of Medicine, Kyungpook National University, Daegu, Korea. dglim@knu.ac.kr |
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Abstract |
BACKGROUND Chronic post-ischemia pain (CPIP) model is reported to represent the complex regional pain syndrome type I. The administration of non-specific free radical scavengers reduced mechanical allodynia, but it is not evident which type of free radical is responsible for the development of CPIP. This study was investigated to elucidate the role of superoxide on the development of CPIP and the relationship with the expression of c-fos gene. METHODS Male Sprague-Dawley rats weighing 290-310 g were housed in one cage with food and water ad libitum. CPIP model was made by placing a tourniquet on the left hindpaw of rats. The tourniquet maintained for 3 hours, then released to allow reperfusion. Thirty minutes before reperfusion, superoxide dismutase (SOD) or normal saline (control group) was injected. Mechanical allodynia and cold allodynia were measured at 1, 3, 5, 7, 14 and 28 days after reperfusion and compared. Also, spinal cord was harvested and the expression of c-fos gene was measured through the real time reverse transcription polymerase chain reaction. RESULTS Superoxide dismutase reduced mechanical allodynia (1, 3, 5 and 14 day) and cold allodynia (1, 3 and 7 day) compared with control rats in left hindpaw. Expression of c-fos was significantly reduced in the SOD rats at the day 14 and 28 compare to the control rats. CONCLUSIONS The administration of superoxide dismutase suppressed the allodynia and c-fos gene expression of CPIP model rats and it may be suggested that the superoxide has an important role in the development of CPIP. |
Key Words:
c-fos gene; complex regional pain syndrome; reperfusion injury; superoxide; superoxide dismutase |
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