CAJ | 학술논문

目的探讨大麻素CB2受体在电针预处理诱导的脑缺血耐受中的作用. 方法实验1:成年雄性SD大鼠40只按随机数字表法分为5组:大脑中动脉闭塞(MCAO)组、电针(EA)+MCAO组、CB2受体拮抗剂(AM630)+EA+MCAO组、AM630的溶剂(V)+EA+MCAO组和AM630+MCAO组(n=8),线拴法制作MCAO模型,EA预处理在模型前2 h给予,AM630或其溶剂在模型前5.5h给予,于模型后72h行神经功能评分和2,3,5-氯化三苯基四氮唑(TTC)染色检测脑梗死容积百分比的变化;实验2:成年雄性SD大鼠40只分组和处理同上,EA预处理在模型前24 h给予,AM630或其溶剂在模型前27.5 h给予,检测指标的时间和方法同实验1;实验3:成年雄性SD大鼠36只按照随机数字表法分为6组:对照组和EA后2、6、12、18、24 h组(n=6).后5组给予EA处理后在不同时间点应用RT-PCR和Western Blot检测各组大鼠右侧大脑中CB2受体的表达.结果实验1:与MCAO组和AM630+MCAO组比较,EA+MCAO组、AM630+EA+MCAO组、V+EA+MCAO组大鼠神经功能评分增高.脑梗死容积百分比降低,差异有统计学意义(P<0.05);实验2:与MCAO组比较.EA+MCAO组和V+EA+MCAO组大鼠神经功能评分增高,脑梗死容积百分比降低.与EA+MCAO组比较,AM630+EA+MCAO组和AM630+MCAO组大鼠神经功能评分降低,脑梗死容积百分比增高,差异均有统计学意义(P<0.05);实验3:与对照组比较,EA后18 h组CB2受体mRNA水平增高,EA后24 h组CB2受体蛋白增高,差异有统计学意义(P<0.05).结论 CB2受体参与了电针预处理诱导的延迟相脑保护作用.
목적 탐토대마소CB2수체재전침예처리유도적뇌결혈내수중적작용. 방법 실험1:성년웅성SD대서40지안수궤수자표법분위5조:대뇌중동맥폐새(MCAO)조、전침(EA)+MCAO조、CB2수체길항제(AM630)+EA+MCAO조、AM630적용제(V)+EA+MCAO조화AM630+MCAO조(n=8),선전법제작MCAO모형,EA예처리재모형전2 h급여,AM630혹기용제재모형전5.5h급여,우모형후72h행신경공능평분화2,3,5-록화삼분기사담서(TTC)염색검측뇌경사용적백분비적변화;실험2:성년웅성SD대서40지분조화처리동상,EA예처리재모형전24 h급여,AM630혹기용제재모형전27.5 h급여,검측지표적시간화방법동실험1;실험3:성년웅성SD대서36지안조수궤수자표법분위6조:대조조화EA후2、6、12、18、24 h조(n=6).후5조급여EA처리후재불동시간점응용RT-PCR화Western Blot검측각조대서우측대뇌중CB2수체적표체.결과 실험1:여MCAO조화AM630+MCAO조비교,EA+MCAO조、AM630+EA+MCAO조、V+EA+MCAO조대서신경공능평분증고.뇌경사용적백분비강저,차이유통계학의의(P<0.05);실험2:여MCAO조비교.EA+MCAO조화V+EA+MCAO조대서신경공능평분증고,뇌경사용적백분비강저.여EA+MCAO조비교,AM630+EA+MCAO조화AM630+MCAO조대서신경공능평분강저,뇌경사용적백분비증고,차이균유통계학의의(P<0.05);실험3:여대조조비교,EA후18 h조CB2수체mRNA수평증고,EA후24 h조CB2수체단백증고,차이유통계학의의(P<0.05).결론 CB2수체삼여료전침예처리유도적연지상뇌보호작용.
Objective To investigate the effect of cannabinoid CB2 receptor on ischemic tolerance of rat models with focal cerebral ischemia induced by electroacupuncture(EA)pretreatment.Methods The first experiment was performed as follows:40 adult male SD rats were randomized into 5 groups(middle cerebral artery occlusion[MCAO]group[vehicle],EA+MCAO group,AM630[the antagonist of CB2 receptor]+EA+MCAO group,V[the solvent of AM630]+EA+MCAO group and AM630+MCAO group,n=8).Suture method was employed to induce th eMCAO models.Pretreatment with EA was given 2h before the model making;pretreatment with AM630 or other solvents were given 5.5 h before the model making.The changes of infarction volume percentage were detected by 2,3,5-triphenoltetrazolium chloride (TTC)staining and neurobehavioral scores were evaluated 72 h after the success of model making.In the second experiment,40 adult male SD rats were performed the same treatment with the first experiment;pretreatment with EA was performed 24h before the model making;pretreatment with AM630 or other solvents were performed 27.5 h before the model making;the measurements and detection times were the same with the first one.In the third experiment,36 adult male SD rats were randomized into 6 groups(n=6):control group and EA-treated groups(2,6,12,18 and 24 h after the treatment). RT-PCR and Western blotting Were employed to detect the expression of CB2 receptor on the right side of rat brain. Results Compared with the vehicle and AM630+MCAO groups,the EA+MCAO group,AM630+EA+MCAO group and V+EA+MCAO group showed significantly higher scores of nerve function and a statistically lower percentage of infarction volume(P<0.05).Compared with the vehicle group,EA+MCAO group and V+EA+MCAO group showed significantly higher neurobehavioral scores and a lower percentage of infarction volume (P<0.05);compared with the EA+MCAO group,the AM630+EA+MCAO group and AM630+MCAO group showed significantly lower neurobehavioral scores and a higher percentage of infarction volume (P<0.05).The mRNA and protein expressions of CB2 receptor were significantly up-regulated in the EA-treatedgroups 18 and 24h after the treatment,respectively,as compared with those in the control group(P<0.05). Conclusion Cannabinoid CB2 receptor involves in the protective effect of delayed tolerance to focal cerebral ischemia induced by pretreatment with EA.