CAJ | 학술논문

目的:研究三七总皂甙(PNS)对吗啡戒断大鼠大脑皮质m2,m5乙酰胆碱受体(AChR)mRNA及蛋白表达的影响,探讨PNS抑制吗啡戒断症状的作用机制.方法:以剂量递增法建立大鼠吗啡依赖模型(MOR组),以腹腔注射(ip)纳洛酮建立催促戒断模型(NAL组),大鼠在给予吗啡的同时,采用3种不同剂量PNS(100、200、400 mg·kg~(-1))灌胃(ig).采用RT-PCR和Western-blot方法分别观察PNS对吗啡依赖及戒断大鼠皮质m2,m5 AChR mRNA及蛋白表达的影响.结果:(1) 慢性吗啡作用使皮质m2,m5 AChR mRNA及m2 AChR蛋白表达明显增加(P<0.01);(2)纳洛酮催促戒断使m2,m5 AChR mRNA及蛋白表达进一步升高(P<0.01);(3) PNS可以剂量依赖性地抑制纳洛酮催促戒断所引起的AChR mRNA及蛋白表达的增强.结论:PNS可通过抑制m2,m5 AChR mRNA及蛋白的表达缓解吗啡戒断症状.
목적:연구삼칠총조대(PNS)대마배계단대서대뇌피질m2,m5을선담감수체(AChR)mRNA급단백표체적영향,탐토PNS억제마배계단증상적작용궤제.방법:이제량체증법건립대서마배의뢰모형(MOR조),이복강주사(ip)납락동건립최촉계단모형(NAL조),대서재급여마배적동시,채용3충불동제량PNS(100、200、400 mg·kg~(-1))관위(ig).채용RT-PCR화Western-blot방법분별관찰PNS대마배의뢰급계단대서피질m2,m5 AChR mRNA급단백표체적영향.결과:(1) 만성마배작용사피질m2,m5 AChR mRNA급m2 AChR단백표체명현증가(P<0.01);(2)납락동최촉계단사m2,m5 AChR mRNA급단백표체진일보승고(P<0.01);(3) PNS가이제량의뢰성지억제납락동최촉계단소인기적AChR mRNA급단백표체적증강.결론:PNS가통과억제m2,m5 AChR mRNA급단백적표체완해마배계단증상.
Objective:To investigate the effects of panax notoginseng(PNS) on m2, m5 AChR mRNA and protein expressions in cortex of morphine dependent and naloxone-precipitated withdrawal rats, and to clarify the mechanism by which PNS attenuated morphine withdrawal syndrome. Methods:Models of morphine physical dependent(MOR group)and withdrawal rats(NAL group)were established by subcutaneous injection of morphine in gradually increasing doses and abdominal cavity injection of naloxone, respectively. The rats were treated with PNS by intragastric administration at different doses(100, 200, 400 mg·kg~(-1)) simultaneously when administrated with morphine. M2, m5 AChR mRNA and protein expressions were detected by RT-PCR and Western-blot, respectively. Results:(1)Chronic morphine treatment increased m2, m5 AChR mRNA and m2 AChR protein expression in cortex(P<0.01). (2) Naloxone increased further m2, m5 AChR mRNA and protein expression in cortex(P<0.01). (3)PNS downregulated dose-dependently m2, m5 AChR mRNA and protein expression induced by naloxone precipitated withdrawal. Conclusion:PNS could alleviate morphine withdrawal symptoms by inhibiting m2, m5 AChR mRNA and protein expression.