大鼠侧脑室注射Apelin-13对急性痛的调节作用及机制

发布时间：2018-02-28 20:32

  本文关键词： Apelin 急性痛 镇痛 酪蛋白激酶Ⅱ NRB亚单位　出处：《中华诊断学电子杂志》2016年04期 　论文类型：期刊论文

【摘要】：目的探讨Apelin-13对大鼠急性痛的调制作用及可能机制。方法简单随机抽样将50只大鼠分为生理盐水组、Apelin-13 0.05μg/g组、Apelin-13 0.1μg/g组、Apelin-13 0.5μg/g组及吗啡组(阳性对照组),每组10只,采用辐射热甩尾法连续监测60 min内大鼠痛阈的变化;同样采用简单随机抽样将40只大鼠分为生理盐水组、Apelin-13 0.5μg/g组、酪蛋白激酶2(CK2)抑制剂四溴苯三唑(TBB)组及Apelin-13+TBB组,每组10只,监测其痛阈的变化。Western Blot法检测海马内CK2表达量及N-甲基-D-天冬氨酸(NMDA)受体NR2B亚单位(P-NR2B S1480)磷酸化水平,研究Apelin-13对急性痛调制作用可能的机制。结果 Apelin-13可显著升高急性痛痛阈,0.5μg/g组给药10 min时甩尾潜伏期变化率(TWL%)达峰值[(50.03±2.71)%],与生理盐水组比较差异有统计学意义(q=18.054,P=0.003),并且此效应呈剂量和时间依赖(F_(Group)=47.729,P=0.000;F_(Time)=205.301,P=0.000)。同时给予CK2抑制剂TBB 10 min时TWL%降至(17.75±1.67)%,低于Apelin-13组,差异有统计学意义(q=6.976,P=0.005)。Western Blot结果显示TBB可明显减弱Apelin-13的作用,CK2α表达量、NR2B亚单位磷酸化水平均下降[(26.92±4.38)%,(39.90±7.40)%],与Apelin-13组[(41.60±6.65)%,(70.83±3.52)%]比较差异有统计学意义(q=5.246,P=0.010;q=9.757,P=0.010)。结论 Apelin-13可能通过CK2促进NMDA受体NR2B亚单位磷酸化,进而在热甩尾急性痛模型中起镇痛作用。
[Abstract]:Objective to investigate the modulation effect of Apelin-13 on acute pain in rats and its possible mechanism. Methods Fifty rats were randomly divided into normal saline group (n = 10), Apelin-13 (0. 5 渭 g / g) group (n = 10) and morphine group (n = 10), Apelin-13 0. 1 渭 g / g group (n = 10) and morphine group (n = 10). The pain threshold of rats during 60 min was continuously monitored by radiation heat tail-flick method, and 40 rats were randomly divided into normal saline group (Apelin-13 0.5 渭 g / g), casein kinase 2 CK2 (TBBB) group and Apelin-13 TBB group (10 rats in each group), and 10 rats in each group were divided into three groups: normal saline group (n = 10), casein kinase 2 (CK2) inhibitor TBBB group (n = 10) and Apelin-13 TBB group (n = 10). Western Blot method was used to detect the expression of CK2 and the phosphorylation of N-methyl-Daspartate receptor NR2B subunit (P-NR2B S1480) in hippocampus. To study the possible mechanism of Apelin-13 on acute pain modulation. Results Apelin-13 could significantly increase the acute pain threshold of 0.5 渭 g / g group and the change rate of tail flick latency was 50.03 卤2.71% at 10 min. There was a significant difference between Apelin-13 group and normal saline group (P 0.003), and there was a significant difference between Apelin-13 group and normal saline group. This effect was dose-dependent and time-dependent. TWL% decreased to 17.75 卤1.67% in CK2 inhibitor TBB 10 min, which was lower than that in Apelin-13 group. The results of Western Blot showed that TBB could obviously attenuate the effect of Apelin-13 on the expression of CK2 伪 and the phosphorylation level of NR2B subunit was decreased [26.92 卤4.38], which was significantly different from that of Apelin-13 group [41.60 卤6.65 + 70.83 卤3.52%]. Conclusion Apelin-13 may promote NMDA receptor through CK2. NR2B subunit phosphorylation, Then the analgesic effect was played in the acute pain model of hot tail flick.
【作者单位】： 济宁医学院神经生物学研究所;
【基金】：2016年地方高校国家级大学生创新创业训练计划项目[201610443048] 济宁医学院青年基金[JYQ14KJ19];济宁医学院大学生创新训练计划项目[CX2015005] 2015年度济宁市医药卫生计划项目[79] 济宁医学院2015年度大学生科研课题
【分类号】：R741
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