急性内脏痛大鼠脊髓背角神经元ERK1／ERK2磷酸化水平的变化  

Changes in ERK1/ERK2 phosphorylation level in spinal dorsal horn neurons in rats with acute visceral pain

作　　者：王立中[1] 邬万新 刘霞[2] 柴荣奎[4] 汤蓓蕾 

机构地区：[1]浙江省嘉兴市妇幼保健院嘉兴市市立三一医院麻醉科,314000 [2]浙江省嘉兴市妇幼保健院嘉兴市市立三一医院妇产科,314000 [3]嘉兴市第一医院病理科 [4]嘉兴学院医学院病理教研室

出　　处：《中华麻醉学杂志》2009年第2期133-135,共3页Chinese Journal of Anesthesiology

基　　金：浙江省医药卫生科学研究基金项目（20068130）;嘉兴市科技计划项目（2006AZ2011）

摘　　要：目的探讨脊髓背角神经元细胞外信号调节激酶（ERK）是否参与急性内脏痛的形成。方法第一部分成年雌性SD大鼠30只，随机分为5组（n=6），假手术组（S组）不行宫颈扩张，UCD25组、UCD50组、UCD75组和UCD100组分别采用25、50、75、100g的强度进行宫颈扩张10s，10min后处死大鼠，采用免疫组化方法测定颈段（C5-8）、胸段（T5-8）、胸腰段（T12-L2）及腰骶段（L6～S1）脊髓背角神经元磷酸化ERK1／ERK2（p-ERK1／ERK2）表达水平。第二部分成年雌性SD大鼠20只，宫颈扩张（强度为75g）10s，于宫颈扩张后10、30、60及120min时分别处死5只大鼠，测定胸腰段（T12-L2）p—ERK1／ERK2表达水平。结果与S组比较，其它各组胸腰段p-ERK1／ERK2表达上调，其中UCD75组和UCD100组最明显（P〈0．05），其他脊髓段p-ERK1／ERK2表达差异无统计学意义（P〉0．05）。宫颈扩张后60min时胸腰段p-ERK1／ERK2表达达高峰（P〈0．05）。结论胸腰段脊髓背角神经元ERK参与了宫颈扩张诱发大鼠急性内脏痛的形成。Objective To investigate whether extracellular signaling-regulated kinases （ERK） in spinal dorsal horn neurons is involved in the development of acute visceral pain. Methods Part T Thirty adult female SD rats were randomly divided into 5 groups （ n = 6 each） ： sham operation group received no uterine cervical distension（UCD）（S）; group UCD25, UCD50, UCD75 and UCD100 received a stimulus of 25, 50, 75 and 100 g UCD for 10 s respectively. After 10 min, the rats were killed. The level of phosphorylated ERK1/ERK2 （p-ERK1/ERK2） in spinal dorsal horn neurons in cervical （ C5-8 ）, thoracic （T5-8 ）, thoracolumbar （T12-L2 ） and lumbosacral （L6-S1） segments was determined by immuno-histochemical method. Part Ⅱ Twenty adult female SD rats received a stimulus of 75 g UCD for 10 s. Five rats were killed at 10, 30, 60 and 120 min after UCD respectively. The expression of p-ERK1/ERK2 in spinal dorsal horn neurons in thoracolumbar （T12-I2 ） segment was determined by immuno-histochemical method. Results The p-ERK1/ERK2 expression in thoracolumbar segments in the 4 UCD groups was significantly up-regulated as compared to S group, with most obvious increase in UCD75 and UCD100 group （P 〈 0.05）. There were no significant differences in p-ERK1/ERK2 expression in the other spinal segments among all the groups （P 〉 0.05）. The p-ERK1/ERK2 expression in thoracolumbar segment peaked at 60 min after UCD （ P 〈 0.05）. Conclusion The ERK in thoracolumbar spinal dorsal horn neurons involves in the development of UCD-induced acute visceral pain in rats.

关 键 词：细胞外信号调节 MAP激酶类 脊髓 疼痛 

分 类 号：R285.5[医药卫生—中药学]