신경병증성 통증모델 쥐에서 리도케인의 ERK 1/2와 CREB 단백질 억제효과
Background: In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2, p38 MAPK, and CREB in the spinal cord, which corre...
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| Published in | Korean journal of anesthesiology Vol. 56; no. 3; pp. 319 - 324 |
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| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | Korean |
| Published |
대한마취통증의학회
30.03.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 2005-6419 2005-7563 |
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| Abstract | Background: In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2, p38 MAPK, and CREB in the spinal cord, which correspond to allodynia in a model of neuropathic pain. The current study was designed to determine if lidocaine had an effect on the development of neuropathic pain in response to SCI. Methods: Male Sprague Dawley rats were anesthetized and then received a L5-L6 spinal nerve ligation (neuropathic rats). The levels of intracellular cell-signaling protein, ERK 1/2 and CREB were then assessed by western blot analysis of samples collected from a sham operated (control) group, a neuropathic pain and normal saline (NP+NS) group, and a neuropathic pain and 5% lidocaine (NP+Lido) group. Results: The increased levels of ERK 1/2 and CREB protein that were observed in the neuropathic pain model were reduced by continuous infusion of 5% lidocaine. Conclusions: The current results suggest that lidocaine therapy may be an effective method of preventing and treating central neuropathic pain following SCI, and that these effects may occur via the reduced expression of ERK 1/2 and CREB in the intracellular cell-signaling pathway. (Korean J Anesthesiol 2009; 56: 319~24) |
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| AbstractList | Background: In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2, p38 MAPK, and CREB in the spinal cord, which correspond to allodynia in a model of neuropathic pain. The current study was designed to determine if lidocaine had an effect on the development of neuropathic pain in response to SCI.
Methods: Male Sprague Dawley rats were anesthetized and then received a L5−L6 spinal nerve ligation (neuropathic rats). The levels of intracellular cell-signaling protein, ERK 1/2 and CREB were then assessed by western blot analysis of samples collected from a sham operated (control) group, a neuropathic pain and normal saline (NP + NS) group, and a neuropathic pain and 5% lidocaine (NP + Lido) group.
Results: The increased levels of ERK 1/2 and CREB protein that were observed in the neuropathic pain model were reduced by continuous infusion of 5% lidocaine.
Conclusions: The current results suggest that lidocaine therapy may be an effective method of preventing and treating central neuropathic pain following SCI, and that these effects may occur via the reduced expression of ERK 1/2 and CREB in the intracellular cell-signaling pathway. KCI Citation Count: 1 Background: In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2, p38 MAPK, and CREB in the spinal cord, which correspond to allodynia in a model of neuropathic pain. The current study was designed to determine if lidocaine had an effect on the development of neuropathic pain in response to SCI. Methods: Male Sprague Dawley rats were anesthetized and then received a L5-L6 spinal nerve ligation (neuropathic rats). The levels of intracellular cell-signaling protein, ERK 1/2 and CREB were then assessed by western blot analysis of samples collected from a sham operated (control) group, a neuropathic pain and normal saline (NP+NS) group, and a neuropathic pain and 5% lidocaine (NP+Lido) group. Results: The increased levels of ERK 1/2 and CREB protein that were observed in the neuropathic pain model were reduced by continuous infusion of 5% lidocaine. Conclusions: The current results suggest that lidocaine therapy may be an effective method of preventing and treating central neuropathic pain following SCI, and that these effects may occur via the reduced expression of ERK 1/2 and CREB in the intracellular cell-signaling pathway. (Korean J Anesthesiol 2009; 56: 319~24) |
| Author | Dae Woo Kim 주진덕 정홍수 Eun Young Shin 전연수 Woo Young Choi 인장혁 김용신 Yeon Soo Jeon Hong Soo Jung 김대우 신은영 최우영 Jang Hyeok In Yong Shin Kim Jin Deok Joo |
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| SubjectTerms | CREB ERK 1/2 Intracellular cell-signaling pathway Lidocaine Neuropathic pain Western blots 마취과학 |
| Title | 신경병증성 통증모델 쥐에서 리도케인의 ERK 1/2와 CREB 단백질 억제효과 |
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