中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
8期
559-563
,共5页
汪丽云%杨婷%钱伟%侯晓华
汪麗雲%楊婷%錢偉%侯曉華
왕려운%양정%전위%후효화
睡眠,快速眼运动%睡眠障碍,内源性%内源性大麻酚类%受体,大麻酚,CB1
睡眠,快速眼運動%睡眠障礙,內源性%內源性大痳酚類%受體,大痳酚,CB1
수면,쾌속안운동%수면장애,내원성%내원성대마분류%수체,대마분,CB1
Sleep,REM%Sleep disorders,intrinsic%Endocannabinoids%Receptor,cannabinoid,CB1
目的 研究中枢内源性大麻素系统是否参与快动眼(REM)睡眠剥夺导致的内脏感觉降低.方法 采用花瓶技术制作大鼠REM睡眠剥夺模型,24只SD大鼠随机分成实验对照组(YC组),睡眠剥夺组(SD组)和睡眠剥夺加大麻素CB1受体拮抗剂利莫那班组(Rim组).睡眠剥夺持续48 h后对各组大鼠行结直肠扩张(CRD),同时用电生理记录仪记录腹壁肌电活动,以反映内脏感觉的变化.分别采用RT-PCR和蛋白质印迹技术测定YC组和SD组大鼠丘脑、脑干、脊髓(腰髓)中CBl受体、脂肪酸酰水解酶(FAAH)和单酰甘油脂肪水解酶(MGL)Mrna和蛋白表达.结果 (1)给予40、60、80 mm Hg(1 mm Hg=0.133 kPa)扩张结直肠后,SD组腹外斜肌放电次数(次:220±94、313 4±162、493±279)均显著低于YC组(次:506 4±223、1053±548、1632 4±249,均P＜0.05);Rim组(次:668±257、1144±93、1653±153)均显著高于SD组(均P＜0.01),Rim组与YC组差异无统计学意义(均P＞0.05).(2)丘脑、脑干、脊髓中CBl受体Mrna以及蛋白表达SD组均显著高于YC组(均P＜0.05),而FAAH、MGL表达量则显著低于YC组(均P＜0.05).结论 REM睡眠剥夺导致的内脏感觉降低可能与中枢内源性大麻素受体表达增加、代谢降低有关.
目的 研究中樞內源性大痳素繫統是否參與快動眼(REM)睡眠剝奪導緻的內髒感覺降低.方法 採用花瓶技術製作大鼠REM睡眠剝奪模型,24隻SD大鼠隨機分成實驗對照組(YC組),睡眠剝奪組(SD組)和睡眠剝奪加大痳素CB1受體拮抗劑利莫那班組(Rim組).睡眠剝奪持續48 h後對各組大鼠行結直腸擴張(CRD),同時用電生理記錄儀記錄腹壁肌電活動,以反映內髒感覺的變化.分彆採用RT-PCR和蛋白質印跡技術測定YC組和SD組大鼠丘腦、腦榦、脊髓(腰髓)中CBl受體、脂肪痠酰水解酶(FAAH)和單酰甘油脂肪水解酶(MGL)Mrna和蛋白錶達.結果 (1)給予40、60、80 mm Hg(1 mm Hg=0.133 kPa)擴張結直腸後,SD組腹外斜肌放電次數(次:220±94、313 4±162、493±279)均顯著低于YC組(次:506 4±223、1053±548、1632 4±249,均P＜0.05);Rim組(次:668±257、1144±93、1653±153)均顯著高于SD組(均P＜0.01),Rim組與YC組差異無統計學意義(均P＞0.05).(2)丘腦、腦榦、脊髓中CBl受體Mrna以及蛋白錶達SD組均顯著高于YC組(均P＜0.05),而FAAH、MGL錶達量則顯著低于YC組(均P＜0.05).結論 REM睡眠剝奪導緻的內髒感覺降低可能與中樞內源性大痳素受體錶達增加、代謝降低有關.
목적 연구중추내원성대마소계통시부삼여쾌동안(REM)수면박탈도치적내장감각강저.방법 채용화병기술제작대서REM수면박탈모형,24지SD대서수궤분성실험대조조(YC조),수면박탈조(SD조)화수면박탈가대마소CB1수체길항제리막나반조(Rim조).수면박탈지속48 h후대각조대서행결직장확장(CRD),동시용전생리기록의기록복벽기전활동,이반영내장감각적변화.분별채용RT-PCR화단백질인적기술측정YC조화SD조대서구뇌、뇌간、척수(요수)중CBl수체、지방산선수해매(FAAH)화단선감유지방수해매(MGL)Mrna화단백표체.결과 (1)급여40、60、80 mm Hg(1 mm Hg=0.133 kPa)확장결직장후,SD조복외사기방전차수(차:220±94、313 4±162、493±279)균현저저우YC조(차:506 4±223、1053±548、1632 4±249,균P＜0.05);Rim조(차:668±257、1144±93、1653±153)균현저고우SD조(균P＜0.01),Rim조여YC조차이무통계학의의(균P＞0.05).(2)구뇌、뇌간、척수중CBl수체Mrna이급단백표체SD조균현저고우YC조(균P＜0.05),이FAAH、MGL표체량칙현저저우YC조(균P＜0.05).결론 REM수면박탈도치적내장감각강저가능여중추내원성대마소수체표체증가、대사강저유관.
objective To study the effects and role of central endocannabinoid system in the mechanism of visceral hyposensitivity induced by rapid eye movement(REM)sleep deprivation.Methods Twenty-four SD rat were divided randomly in to 3 groups:cage-yoked group(YC Group,experimental control group),REM sleep deprivation group(SD Group)exposed to REM sleep deprivation by means of flower pot technique lasting for 48 hours,and Rim Group,receiving rimonabant,a cannabinoid antagonist,after REM sleep deprivation.48 hours after the sleep deprivation abdominal eleetromyogram in response to colorectal distension(CRD)was recorded to asses t11e visceral sensitivity.Then the rats were killed with their central nervous system taken out.RT-PCR and Western blotting were used to detect the RNA and protein expression of cannabinoid receptor CBl,fatty acid amide hydrolase(FAAH),and monoaeylglyeerol lipase(MGL)in the thaiamus,brain stem,and spinal cord.Results (1)Under the pressures of 40,60,and 80 mm Hg.the abdominal electrical activity frequencies of external oblique muscle responding to CRD in SD Group were(220±94),(313±162),and(493± 279)times respectively,all significantly lower than those in YC Group[(506±223),(1053±548),and(1632±249)times respectively,all P＜0.05],and those of Rim Group were(668±257),(1144±93),and(1653±153)times respectively,all signifieantly higher than those of SD Group(a11 P＜0.05),but not significantly different from those of YC Group.(2)The RNA and protein expression levels of CB1 receptor in the thalamus,brain stem,and spinal cord of SD Group were all significantly higller than those of YC Group(all P＜0.05),while the RNA and protein expression levels of FAAH and MGL in the thalamus and spinal cord of SD Group were all significantly lower than those of YC Group(all P＜0.05).Conclusion The visceral hypesensitivity induced by REM sleep deprivation may be associated with the increase of expression of CNS endocannabinoid receptor and decrease of its metabolism.
