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急性内脏痛大鼠脊髓背角神经元ERK1/ERK2磷酸化水平的变化
引用本文:王立中,邬万新,刘霞,柴荣奎,汤蓓蕾. 急性内脏痛大鼠脊髓背角神经元ERK1/ERK2磷酸化水平的变化[J]. 中华麻醉学杂志, 2009, 29(2). DOI: 10.3760/cma.j.issn.0254-1416.2009.02.010
作者姓名:王立中  邬万新  刘霞  柴荣奎  汤蓓蕾
作者单位:1. 嘉兴市市立三一医院麻醉科,浙江省嘉兴市妇幼保健院,314000
2. 嘉兴市第一医院病理科
3. 嘉兴市市立三一医院妇产科,浙江省嘉兴市妇幼保健院,314000
4. 嘉兴学院医学院病理教研室
基金项目:浙江省医药卫生科学研究基金,嘉兴市科技计划 
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、100 g的强度进行宫颈扩张10 s,10 min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75 g)10 s,于宫颈扩张后10、30、60及120 min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60 min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.

关 键 词:细胞外信号调节MAP激酶类  脊髓  疼痛

Changes in ERK1/ERK2 phosphorylation level in spinal dorsal horn neurons in rats with acute visceral pain
Abstract:Objective To inyestignte whether extracellular signaling-regulated kinases (ERK) in spinal dorsal horn neurons is involved in the development of acute visceral pain. Methods Part Ⅰ Thirty adult female SD rats were randomly divided into 5 groups (n=6 each):sham operation group received no uterine cervical disteneion(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-L2) segment was determined by immuno-histochemical method. Results The p-ERK1/ERK2 expression in thoraeolumbar 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.
Keywords:Extracellular signal-regulated MAP kinases  Spinal cord  Pain
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