CAJ | 학술논문

目的建立大鼠β-淀粉样肽[Aβ(25-35)]诱导的痴呆模型,探讨知母总皂苷在阿耳茨海默病(AD)发病机制中的作用.方法SD大鼠60只,采用脑立体定位技术在大鼠单侧侧脑室一次性注射老化的Aβ(25-35)建立实验性AD模型.手术24 h后,大鼠经灌胃分别给予3种剂量的知母总皂苷和EGB761,模型组和空白组给予等剂量的蒸馏水,1次/1 d,连续14 d.在给予Aβ(25-35)后的第8天,应用Morris水迷宫法测定大鼠的学习记忆功能,造模后第14天断头取脑,测定脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)和总抗氧化能力.结果与空白对照组相比,模型组大鼠空间学习记忆能力明显减弱,寻找平台潜伏期明显延长(P＜0.01);脑组织SOD、总抗氧化能力明显降低(P＜0.01),而MDA明显升高(P＜0.05).与模型组比较,给予知母总皂苷治疗后的大鼠学习记忆功能障碍得到明显改善,潜伏期显著缩短(P＜0.05),SOD活力显著提高(P＜0.05),总抗氧化能力也显著增强(P＜0.05),MDA水平明显降低(P＜0.05).结论知母总皂苷可明显改善AD模型大鼠的学习记忆功能,同时可提高模型大鼠的抗过氧化能力,这有可能是其改善学习记忆的原因之一.
목적건립대서β-정분양태[Aβ(25-35)]유도적치태모형,탐토지모총조감재아이자해묵병(AD)발병궤제중적작용.방법SD대서60지,채용뇌입체정위기술재대서단측측뇌실일차성주사노화적Aβ(25-35)건립실험성AD모형.수술24 h후,대서경관위분별급여3충제량적지모총조감화EGB761,모형조화공백조급여등제량적증류수,1차/1 d,련속14 d.재급여Aβ(25-35)후적제8천,응용Morris수미궁법측정대서적학습기억공능,조모후제14천단두취뇌,측정뇌조직초양화물기화매(SOD)、병이철(MDA)화총항양화능력.결과여공백대조조상비,모형조대서공간학습기억능력명현감약,심조평태잠복기명현연장(P＜0.01);뇌조직SOD、총항양화능력명현강저(P＜0.01),이MDA명현승고(P＜0.05).여모형조비교,급여지모총조감치료후적대서학습기억공능장애득도명현개선,잠복기현저축단(P＜0.05),SOD활력현저제고(P＜0.05),총항양화능력야현저증강(P＜0.05),MDA수평명현강저(P＜0.05).결론지모총조감가명현개선AD모형대서적학습기억공능,동시가제고모형대서적항과양화능력,저유가능시기개선학습기억적원인지일.
Objective To investigate the effects of timosaponins, one group of the two major components of A nemarrhean asphodeloides Bge, on the learning and memory capacities of rats with dementia induced by amyloid β-peptide (25-35) [Aβ(25-35)]. Methods Sixty SD rats were randomized into 6 groups (n=10) and except for those in the control group, all other rats were subjected to lateral cerebral ventriclar injection of aggregated Aβ (25-35) to prepare rat models of dementia. Twenty four hours after the injection, the rats received intragastric administration of timosaponins at 3 different doses (treatment group) or Ginkgo biloba extract EGB761 on a daily basis for 14 consecutive days. From postoperative days 8 to 14 after Aβ (25-35) injection, Morris water maze test was performed to evaluate the effects of Aβ (25-35) and the therapeutic agents timosaponins on the learning and memory capacity of the rats. On day 14, the level of malonaldehyde (MDA), superoxide dismutase (SOD) activity and total antioxidation capacity in the brain tissue of the rats were measured. Results Aβ (25-35) induced significant learning and memory impairment in the rats, which had lowered SOD activity and total antioxidation capacity (P＜0.01) with elevated MDA level (P＜0.05). Compared with the rats in dementia model group, those receiving timosaponin treatment at different doses all manifested alleviation of learning and memory impairment (P＜0.05), with enhanced SOD activity (P＜0.05) and total antioxidation capacity (P＜0.01) and reduced MDA level (P＜0.05) in the brain tissue. Conclusion Timosaponins can remarkably enhance the learning and memory capacities in rats with Aβ (25-35) -induced dementia, presumably in relation to their actions to promote the scavenging of the free radicals.