CAJ | 학술논문

目的：探讨艾灸治疗阿尔茨海默病(Alzheimer's disease，AD)的作用机制。方法：40只15月龄健康雄性SD大鼠，随机分为正常组、模型组、艾灸组及假手术组。模型组及艾灸组大鼠采用双侧海马立体定向注射聚集态Aβ25-35制作AD模型，假手术组大鼠双侧海马区注射等量生理盐水。造模成功后，在艾灸组大鼠的“肾俞”、“足三里”与“百会”穴上方2-3cm处施予温和灸治疗。正常组大鼠不做任何处理。Morris水迷宫法测定其学习记忆能力，免疫组化法观察艾灸对AD大鼠海马区细胞凋亡相关因子Bcl-2、Bax、Caspase-3表达的影响。结果：模型组大鼠5天逃避潜伏期，后3天逃避潜伏期均明显延长，跨越原平台位置的次数明显减少，大鼠海马区Bax、Caspase-3表达较正常组、假手术组明显升高，Bcl-2表达明显降低（P<0.01）。艾灸组大鼠5天逃避潜伏期和后3天逃避潜伏期均明显缩短，跨越原平台位置的次数明显增多，大鼠海马区Bax、Caspase-3表达较模型组显著下降，Bcl-2表达显著升高（P<0.01）。结论：艾灸治疗AD的作用机制，可能是通过减轻促凋亡蛋白Bax、Caspase-3的释放,促进抗凋亡蛋白Bcl-2的产生，从而改善Aβ所致的大鼠学习记忆障碍。
목적：탐토애구치료아이자해묵병(Alzheimer's disease，AD)적작용궤제。방법：40지15월령건강웅성SD대서，수궤분위정상조、모형조、애구조급가수술조。모형조급애구조대서채용쌍측해마입체정향주사취집태Aβ25-35제작AD모형，가수술조대서쌍측해마구주사등량생리염수。조모성공후，재애구조대서적“신유”、“족삼리”여“백회”혈상방2-3cm처시여온화구치료。정상조대서불주임하처리。Morris수미궁법측정기학습기억능력，면역조화법관찰애구대AD대서해마구세포조망상관인자Bcl-2、Bax、Caspase-3표체적영향。결과：모형조대서5천도피잠복기，후3천도피잠복기균명현연장，과월원평태위치적차수명현감소，대서해마구Bax、Caspase-3표체교정상조、가수술조명현승고，Bcl-2표체명현강저（P<0.01）。애구조대서5천도피잠복기화후3천도피잠복기균명현축단，과월원평태위치적차수명현증다，대서해마구Bax、Caspase-3표체교모형조현저하강，Bcl-2표체현저승고（P<0.01）。결론：애구치료AD적작용궤제，가능시통과감경촉조망단백Bax、Caspase-3적석방,촉진항조망단백Bcl-2적산생，종이개선Aβ소치적대서학습기억장애。
This study was aimed to probe into the mechanism of moxibustion in the treatment of Alzheimer’s disease (AD). A total of 40 male 15-month-old SD rats were randomly divided into the normal group, model group, moxibustion group and sham-operation group. Stereotactic injection of agglutinated Aβ25-35 into rat’s bilateral hippocampus was used to prepare AD models. Equal amount of normal saline was injected to rat’s bilateral hippocampus in the sham-operation group. Model rats were treated by moxibustion at the distance of 2-3 cm above points of‘BL23-Shenshu’, ‘ST36-Zusanli’ and ‘GV20-Baihui’. No intervention was given to rats in the normal group. The learning and memory ability was detected by Morris water maze test. Changes on expressions of Bcl-2, Bax and Caspase-3 of hippocampus zone were detected by immunohistochemical method. The results showed that in the model group, the average escape latency of five days and the last three days were significantly lengthened. And the times across the platform position were significantly reduced. Compared with the normal group and the sham-operation group, expressions of Bax and Caspase-3 in the hippocampus were significantly increased, and the expression of Bcl-2 was obviously decreased (P < 0.01). In the moxibustion group, the average escape latency of five days and the last three days were shortened obviously, and the times across the platform position were significantly increased. Compared with the model group, expressions of Bax and Caspase-3 were significantly reduced, and the expression of Bcl-2 was significantly increased (P < 0.01). It was concluded that the action mechanism of AD treatment with moxibustion may be through the reducing of proapoptotic protein Bax and Caspase-3 releasing, promoting the releasing of anti-apoptotic protein Bcl-2, so as to improve the learning and memory impairment caused by Aβ.