CAJ | 학술논문

目的观察艾灸对阿尔茨海默病(Alzheimer's disease,AD)大鼠学习记忆能力及海马CA1区神经细胞超微结构的影响,探讨其治疗AD的作用机制.方法 40只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β淀粉样蛋白(Aβ)25-35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,艾灸组大鼠于"肾俞""足三里"与"百会"穴位上方2~3 cm处施予温和灸治疗.正常组大鼠不做任何处理.Morris水迷宫实验检测大鼠学习记忆能力,透射电镜观察大鼠海马CA1区神经细胞超微结构.结果模型组大鼠5 d逃避潜伏期、后3 d逃避潜伏期均明显延长,跨越原平台位置次数均明显减少;大鼠海马CA1区神经元体积缩小,形态不规则,线粒体肿胀,基质清淡、有空泡,数目减少,可见线粒体嵴呈畸形样改变,内质网扩张,脂褐素沉积增多.经艾灸治疗后,艾灸组大鼠5 d逃避潜伏期和后3 d逃避潜伏期均明显缩短,跨越原平台位置次数均明显增多;大鼠海马CA1区神经细胞水肿明显减轻,内质网扩张明显改善,线粒体肿胀明显减轻.结论艾灸治疗可促进脑内神经细胞的修复,从而改善Aβ所致大鼠学习记忆障碍.
목적 관찰애구대아이자해묵병(Alzheimer's disease,AD)대서학습기억능력급해마CA1구신경세포초미결구적영향,탐토기치료AD적작용궤제.방법 40지SD대서수궤분위정상조、모형조、애구조급가수술조.모형조급애구조대서채용쌍측해마입체정향주사취집태β정분양단백(Aβ)25-35제작AD모형,가수술조대서쌍측해마구주사등량생리염수.조모성공후,애구조대서우"신유""족삼리"여"백회"혈위상방2~3 cm처시여온화구치료.정상조대서불주임하처리.Morris수미궁실험검측대서학습기억능력,투사전경관찰대서해마CA1구신경세포초미결구.결과 모형조대서5 d도피잠복기、후3 d도피잠복기균명현연장,과월원평태위치차수균명현감소;대서해마CA1구신경원체적축소,형태불규칙,선립체종창,기질청담、유공포,수목감소,가견선립체척정기형양개변,내질망확장,지갈소침적증다.경애구치료후,애구조대서5 d도피잠복기화후3 d도피잠복기균명현축단,과월원평태위치차수균명현증다;대서해마CA1구신경세포수종명현감경,내질망확장명현개선,선립체종창명현감경.결론 애구치료가촉진뇌내신경세포적수복,종이개선Aβ소치대서학습기억장애.
Objective To observe the effects of moxibustion on learning and memory ability and nerve cell ultrastructure in CA1 region of hippocampus of rats with Alzheimer's disease (AD);To discuss its mechanism of action to AD.Methods A total of 40 male SD mice was randomly divided into normal group, model group, moxibustion group and sham-operation group. Stereotactic injection agglutinated Aβ25-35 into bilateral hippocampus of rats in model group and moxibustion group to prepare AD models. Rats in moxibustion group were treated by moxibustion at the points which were located above 2-3 cm away from "Shenshu", "Zusanli" and "Baihui". Rats in normal group received no treatment. The learning and memory ability was detected by Morris water maze test. Morphological changes of rat nerve cell ultra structure in hippocampal CA1 region were observed by transmission electron microscope.Results In model group, the average escape latency of five days and the last three days was significantly lengthened, and the times across the platform position significantly decreased. Transmission electron microscope indicated nerve cell structures were damaged and displayed unclearly;mitochondrion swelled, even mitochondrial crista was abnormal and deformed, endoplasmic reticulum of inter organelle expanded and the deposition of lipofuscin increased. After the treatment by moxibustion, the average escape latency of five days and the last three days was shortened obviously, and the times across the platform position significantly increased. In moxibustion group, the edema of nerve cells significantly decreased;dilation of endoplasmic reticulum and mitochondria swelling significantly improved;golgi bodies, mitochondria and ribosomes obviously increased in comparison with the model group. Conclusion Moxibustion can improve the learning and memory impairment caused by Aβ by promoting repairing of nerve cells in brain.