医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2014年
11期
1446-1449
,共4页
吗啡%μ阿片受体%卵巢细胞%细胞外信号调节激酶%磷酸化
嗎啡%μ阿片受體%卵巢細胞%細胞外信號調節激酶%燐痠化
마배%μ아편수체%란소세포%세포외신호조절격매%린산화
Morphine%μ opioid receptor%Ovary cells%ERK%Phosphorylation
目的:利用表达μ阿片受体的中国仓鼠卵巢细胞,研究吗啡急慢性处理下对细胞外信号调节激酶( ERK)磷酸化的影响。方法免疫印迹检测磷酸化ERK水平,获取1 h急性处理的ERK磷酸化变化时程和36 h慢性处理以及纳洛酮催促下的ERK磷酸化变化。结果1μmol·L-1吗啡可以快速诱导ERK磷酸化水平短暂升高,5 min时达峰( P〈0.01),吗啡诱导的ERK磷酸化水平升高具有显著的浓度依赖性。10μmol·L-1吗啡慢性处理36 h后ERK磷酸化水平与对照组比较,差异无统计学意义,但纳洛酮急性催促5或10 min均导致ERK磷酸化显著下降(与对照比较,P〈0.01)。结论吗啡急慢性刺激下以及纳洛酮催促下ERK磷酸化表现出不同的变化形式,提示μ阿片受体介导下ERK相关的信号通路发生了代偿。
目的:利用錶達μ阿片受體的中國倉鼠卵巢細胞,研究嗎啡急慢性處理下對細胞外信號調節激酶( ERK)燐痠化的影響。方法免疫印跡檢測燐痠化ERK水平,穫取1 h急性處理的ERK燐痠化變化時程和36 h慢性處理以及納洛酮催促下的ERK燐痠化變化。結果1μmol·L-1嗎啡可以快速誘導ERK燐痠化水平短暫升高,5 min時達峰( P〈0.01),嗎啡誘導的ERK燐痠化水平升高具有顯著的濃度依賴性。10μmol·L-1嗎啡慢性處理36 h後ERK燐痠化水平與對照組比較,差異無統計學意義,但納洛酮急性催促5或10 min均導緻ERK燐痠化顯著下降(與對照比較,P〈0.01)。結論嗎啡急慢性刺激下以及納洛酮催促下ERK燐痠化錶現齣不同的變化形式,提示μ阿片受體介導下ERK相關的信號通路髮生瞭代償。
목적:이용표체μ아편수체적중국창서란소세포,연구마배급만성처리하대세포외신호조절격매( ERK)린산화적영향。방법면역인적검측린산화ERK수평,획취1 h급성처리적ERK린산화변화시정화36 h만성처리이급납락동최촉하적ERK린산화변화。결과1μmol·L-1마배가이쾌속유도ERK린산화수평단잠승고,5 min시체봉( P〈0.01),마배유도적ERK린산화수평승고구유현저적농도의뢰성。10μmol·L-1마배만성처리36 h후ERK린산화수평여대조조비교,차이무통계학의의,단납락동급성최촉5혹10 min균도치ERK린산화현저하강(여대조비교,P〈0.01)。결론마배급만성자격하이급납락동최촉하ERK린산화표현출불동적변화형식,제시μ아편수체개도하ERK상관적신호통로발생료대상。
Objective To study the phosphorylation mode of extracellular regulated kinase( ERK)induced by acute and chronic morphine treatment on Chinese hamster ovary( CHO)cells expressed withμopioid receptors. Methods The time course of ERK phosphorylation 1 h and 36 h after morphine exposure as well as naloxone-precipitated withdrawal was detected by immunobloting. Results A transient enhancement of ERK phosphorylation was induced by 1 μmol · L-1 morphine with the peak effect at 5 min(P〈0. 01),and the effect was dose-dependent. No difference in ERK phosphorylation was found after 36h of treatment with 10 μmol · L-1 morphine compared with the control. However,5 or 10 min-naloxone precipitation induced remarkable decrease in ERK phosphorylation compared with the control(P〈0. 01). Conclusion Different changes of ERK phosphorylation were found under acute and chronic morphine treatment and naloxone precipitation,indicating a compensation of ERK related pathway induced byμ opioid receptors.