本文關鍵詞： Apelin 急性痛 鎮(zhèn)痛 酪蛋白激酶Ⅱ NRB亞單位　出處：《中華診斷學電子雜志》2016年04期 　論文類型：期刊論文

【摘要】：目的探討Apelin-13對大鼠急性痛的調(diào)制作用及可能機制。方法簡單隨機抽樣將50只大鼠分為生理鹽水組、Apelin-13 0.05μg/g組、Apelin-13 0.1μg/g組、Apelin-13 0.5μg/g組及嗎啡組(陽性對照組),每組10只,采用輻射熱甩尾法連續(xù)監(jiān)測60 min內(nèi)大鼠痛閾的變化;同樣采用簡單隨機抽樣將40只大鼠分為生理鹽水組、Apelin-13 0.5μg/g組、酪蛋白激酶2(CK2)抑制劑四溴苯三唑(TBB)組及Apelin-13+TBB組,每組10只,監(jiān)測其痛閾的變化。Western Blot法檢測海馬內(nèi)CK2表達量及N-甲基-D-天冬氨酸(NMDA)受體NR2B亞單位(P-NR2B S1480)磷酸化水平,研究Apelin-13對急性痛調(diào)制作用可能的機制。結(jié)果 Apelin-13可顯著升高急性痛痛閾,0.5μg/g組給藥10 min時甩尾潛伏期變化率(TWL%)達峰值[(50.03±2.71)%],與生理鹽水組比較差異有統(tǒng)計學意義(q=18.054,P=0.003),并且此效應呈劑量和時間依賴(F_(Group)=47.729,P=0.000;F_(Time)=205.301,P=0.000)。同時給予CK2抑制劑TBB 10 min時TWL%降至(17.75±1.67)%,低于Apelin-13組,差異有統(tǒng)計學意義(q=6.976,P=0.005)。Western Blot結(jié)果顯示TBB可明顯減弱Apelin-13的作用,CK2α表達量、NR2B亞單位磷酸化水平均下降[(26.92±4.38)%,(39.90±7.40)%],與Apelin-13組[(41.60±6.65)%,(70.83±3.52)%]比較差異有統(tǒng)計學意義(q=5.246,P=0.010;q=9.757,P=0.010)。結(jié)論 Apelin-13可能通過CK2促進NMDA受體NR2B亞單位磷酸化,進而在熱甩尾急性痛模型中起鎮(zhèn)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 鹵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 鹵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 偽 and the phosphorylation level of NR2B subunit was decreased [26.92 鹵4.38], which was significantly different from that of Apelin-13 group [41.60 鹵6.65 + 70.83 鹵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.
【作者單位】： 濟寧醫(yī)學院神經(jīng)生物學研究所;
【基金】：2016年地方高校國家級大學生創(chuàng)新創(chuàng)業(yè)訓練計劃項目[201610443048] 濟寧醫(yī)學院青年基金[JYQ14KJ19];濟寧醫(yī)學院大學生創(chuàng)新訓練計劃項目[CX2015005] 2015年度濟寧市醫(yī)藥衛(wèi)生計劃項目[79] 濟寧醫(yī)學院2015年度大學生科研課題
【分類號】：R741
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本文編號：1548840