临床麻醉学杂志
臨床痳醉學雜誌
림상마취학잡지
THE JOURNAL OF CLINICAL ANESTHESIOLOGY
2010年
2期
151-153
,共3页
神经病理性疼痛%脊髓%丝裂原激活/细胞外信号调节激酶-细胞外信号调节蛋白激酶%核转录因子κB
神經病理性疼痛%脊髓%絲裂原激活/細胞外信號調節激酶-細胞外信號調節蛋白激酶%覈轉錄因子κB
신경병이성동통%척수%사렬원격활/세포외신호조절격매-세포외신호조절단백격매%핵전록인자κB
Neuropathtic pain%Spinal cord%Mitogen-activated protein kinase%Nuclear factor kappa B
目的 研究神经病理性疼痛大鼠脊髓中丝裂原激活/细胞外信号调节激酶-细胞外信号调节蛋白激酶(MEK-ERK)与核转录因子κB(NF-κB)信号途径的变化,探讨神经元和星形胶质细胞激活过程中信号途径的变化及意义.方法 12只雌性SD大鼠(体重150～200 g)随机均分为坐骨神经保留性神经损伤组(SNI组)和对照组(C组).分别于术前3 d、术后即刻、术后1、3、5、7、9、11 d测定大鼠对机械刺激产生缩腿反应的次数.术后11 d测定缩腿反应的次数后,每组取3只大鼠用于灌注,应用免疫组织化学方法检测脊髓丝裂原激活/细胞外信号调节激酶(MEK)、磷酸化丝裂原激活/细胞外信号调节激酶(p-MEK)、磷酸化细胞外信号调节蛋白激(p-ERK)、NF-κB的表达.另3只大鼠断头处死后分离L_(4～6)脊髓,提取大鼠脊髓的蛋白质,应用Western Blot方法检测p-MEK、p-ERK、NF-κB表达.结果 SNI组p-MEK、p-ERK、NF-κB表达高于C组(P<0.05).MEK表达于胞浆,p-MEK表达于细胞核;p-ERK主要表达于星形胶质细胞.结论 在神经病理性疼痛大鼠脊髓中,星形胶质细胞MEK-ERK信号途径被激活,脊髓背角深层神经元的NF-κB处于激活状态.
目的 研究神經病理性疼痛大鼠脊髓中絲裂原激活/細胞外信號調節激酶-細胞外信號調節蛋白激酶(MEK-ERK)與覈轉錄因子κB(NF-κB)信號途徑的變化,探討神經元和星形膠質細胞激活過程中信號途徑的變化及意義.方法 12隻雌性SD大鼠(體重150～200 g)隨機均分為坐骨神經保留性神經損傷組(SNI組)和對照組(C組).分彆于術前3 d、術後即刻、術後1、3、5、7、9、11 d測定大鼠對機械刺激產生縮腿反應的次數.術後11 d測定縮腿反應的次數後,每組取3隻大鼠用于灌註,應用免疫組織化學方法檢測脊髓絲裂原激活/細胞外信號調節激酶(MEK)、燐痠化絲裂原激活/細胞外信號調節激酶(p-MEK)、燐痠化細胞外信號調節蛋白激(p-ERK)、NF-κB的錶達.另3隻大鼠斷頭處死後分離L_(4～6)脊髓,提取大鼠脊髓的蛋白質,應用Western Blot方法檢測p-MEK、p-ERK、NF-κB錶達.結果 SNI組p-MEK、p-ERK、NF-κB錶達高于C組(P<0.05).MEK錶達于胞漿,p-MEK錶達于細胞覈;p-ERK主要錶達于星形膠質細胞.結論 在神經病理性疼痛大鼠脊髓中,星形膠質細胞MEK-ERK信號途徑被激活,脊髓揹角深層神經元的NF-κB處于激活狀態.
목적 연구신경병이성동통대서척수중사렬원격활/세포외신호조절격매-세포외신호조절단백격매(MEK-ERK)여핵전록인자κB(NF-κB)신호도경적변화,탐토신경원화성형효질세포격활과정중신호도경적변화급의의.방법 12지자성SD대서(체중150～200 g)수궤균분위좌골신경보류성신경손상조(SNI조)화대조조(C조).분별우술전3 d、술후즉각、술후1、3、5、7、9、11 d측정대서대궤계자격산생축퇴반응적차수.술후11 d측정축퇴반응적차수후,매조취3지대서용우관주,응용면역조직화학방법검측척수사렬원격활/세포외신호조절격매(MEK)、린산화사렬원격활/세포외신호조절격매(p-MEK)、린산화세포외신호조절단백격(p-ERK)、NF-κB적표체.령3지대서단두처사후분리L_(4～6)척수,제취대서척수적단백질,응용Western Blot방법검측p-MEK、p-ERK、NF-κB표체.결과 SNI조p-MEK、p-ERK、NF-κB표체고우C조(P<0.05).MEK표체우포장,p-MEK표체우세포핵;p-ERK주요표체우성형효질세포.결론 재신경병이성동통대서척수중,성형효질세포MEK-ERK신호도경피격활,척수배각심층신경원적NF-κB처우격활상태.
Objective To investigate the signaling pathways involved in the activation of neuron and glia in spinal cord in rats with neuropathic pain. Methods Twelve female SD rats (weighted 150 to 200 g) were randomized into two groups of spared nerve injury(group SNI) and control(group C). Surgery was performed to build model of SNI neuropathic pain in group SNI. Foot-lift response frequency to mechanical stimulation for ipsilateral hindpaw was assessed by 12 g and 2 g touch stimulator at different times. On the 11~(th) day after operation, 3 rats from each group were fixed by perfusion and the expressions of mitogen-activated/extracellular signal-regulated kinase (MEK), p-mitogen-activated/extracellular signal-regulated kinase (p-MEK), p-extracellular regulated protein kinase(p-ERK) and nuclear factor kappa B (NF-κB) were detected by immunohistochemistry method. And proteins from ipsilateral LA-6 spinal cord in other 3 rats from each group were extracted for Western Blot analysis. Western Blot and immunohistochemistry were performed with antibodies specific for MEK, p-MEK, pERK and NF-κB. Results All rats in group SNI developed a relative unchangeable mechanical allodynia since the 5~(th) day after operation. The results of immunohistochemistry method showed that the expression of MEK was mainly in cytoplasm, p-MEK in cell nuclear, p-ERK in astrocyte and NF-κB in neuron according to morphologic observation. Western Blot analysis indicated that the expressions of p-MEK, p-ERK and NF-κB in group SNI were increased significantly compared with those in group C(P<0. 05). Conclusion In the spinal cord of rats with neuropathic pain, MEK-ERK signaling pathway is activated in astrocytes and NF-κB in neurons, which may contribute to the development of neuropathic pain.
