CAJ | 학술논문

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.
목적 탐토척수배각신경원세포외신호조절격매(ERK)시부삼여급성내장통적형성.방법 제일부분성년자성SD대서30지,수궤분위5조(n=6),가수술조(S조)불행궁경확장,UCD25조、UCD50조、UCD75조화UCD100조분별채용25、50、75、100 g적강도진행궁경확장10 s,10 min후처사대서,채용면역조화방법측정경단(C5～8)、흉단(T5～8)、흉요단(T12～L2)급요저단(L6～S1)척수배각신경원린산화ERK1/ERK2(p-ERK1/ERK2)표체수평.제이부분성년자성SD대서20지,궁경확장(강도위75 g)10 s,우궁경확장후10、30、60급120 min시분별처사5지대서,측정흉요단(T12～L2)p-ERK1/ERK2표체수평.결과 여S조비교,기타각조흉요단p-ERK1/ERK2표체상조,기중UCD75조화UCD100조최명현(P<0.05),기타척수단p-ERK1/ERK2표체차이무통계학의의(P>0.05).궁경확장후60 min시흉요단p-ERK1/ERK2표체체고봉(P<0.05).결론 흉요단척수배각신경원ERK삼여료궁경확장유발대서급성내장통적형성.
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.