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 inKorean journal of anesthesiology Vol. 56; no. 3; pp. 319 - 324
Main Authors 주진덕, Jin Deok Joo, 인장혁, Jang Hyeok In, 정홍수, Hong Soo Jung, 김용신, Yong Shin Kim, 김대우, Dae Woo Kim, 최우영, Woo Young Choi, 신은영, Eun Young Shin, 전연수, Yeon Soo Jeon
Format Journal Article
LanguageKorean
Published 대한마취통증의학회 30.03.2009
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Online AccessGet full text
ISSN2005-6419
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)
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
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Title 신경병증성 통증모델 쥐에서 리도케인의 ERK 1/2와 CREB 단백질 억제효과
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