CAJ | 학술논문

目的：探讨地黄饮子对阿尔茨海默病（Alzheimer's disease，AD）小鼠学习记忆能力及脑能量代谢的影响。方法雄性APPsw/PS1ΔE9转基因小鼠60只，按照随机数字表法随机分为模型组、阳性药（安理申）组、地黄饮子高、中、低剂量组，每组12只；以12只同背景、月龄的C57BL/6J小鼠为正常对照组。小鼠4月龄开始灌胃给药，给药时间150 d。检测小鼠空间学习记忆、被动回避学习记忆能力；测定小鼠脑内能荷（EC）变化、呼吸链复合物I、II和IV活性、Na＋-K＋ATP酶、Ca2＋ATP酶活性、线粒体膜电位。结果模型组小鼠学习记忆能力、脑EC、呼吸链复合物I、II和IV活性、Na＋-K＋ATP酶、Ca2＋ATP酶活性及线粒体膜电位[分别为（0.39±0.02）μOD/(min?μg)、（3.28±0.37）μOD/(min?μg)、（0.19±0.04）mOD/(min?μg)、（0.26±0.03）mOD/(min?μg)、（0.19±0.02）mOD/(min?μg)、（0.30±0.03）mOD/(min?μg)、（3.49±0.73）mOD/(min?μg)]较正常对照组[分别为（0.57±0.06）μOD/（min?μg、（8.74±1.57）μOD/(min?μg)、（0.43±0.02）mOD/(min?μg)、（0.69±0.02）mOD/(min?μg)、（0.65±0.02）、（0.51±0.01）、（7.41±1.28）]降低（P＜0.01）；与模型组比较，地黄饮子可显著改善AD小鼠学习记忆能力，提高脑EC值、呼吸链复合物I和IV活性、Na＋-K＋ATP酶、Ca2＋ATP酶活性与线粒体膜电位[分别为（0.57±0.07）、（8.42±1.74）μOD/(min?μg)、（0.64±0.03）mOD/(min?μg)、（0.68±0.04）、（0.55±0.01）、（6.69±1.03），（P＜0.01或0.05）]。结论地黄饮子通过保护线粒体，提高AD小鼠脑能量代谢，改善学习记忆能力。
목적：탐토지황음자대아이자해묵병（Alzheimer's disease，AD）소서학습기억능력급뇌능량대사적영향。방법웅성APPsw/PS1ΔE9전기인소서60지，안조수궤수자표법수궤분위모형조、양성약（안리신）조、지황음자고、중、저제량조，매조12지；이12지동배경、월령적C57BL/6J소서위정상대조조。소서4월령개시관위급약，급약시간150 d。검측소서공간학습기억、피동회피학습기억능력；측정소서뇌내능하（EC）변화、호흡련복합물I、II화IV활성、Na＋-K＋ATP매、Ca2＋ATP매활성、선립체막전위。결과모형조소서학습기억능력、뇌EC、호흡련복합물I、II화IV활성、Na＋-K＋ATP매、Ca2＋ATP매활성급선립체막전위[분별위（0.39±0.02）μOD/(min?μg)、（3.28±0.37）μOD/(min?μg)、（0.19±0.04）mOD/(min?μg)、（0.26±0.03）mOD/(min?μg)、（0.19±0.02）mOD/(min?μg)、（0.30±0.03）mOD/(min?μg)、（3.49±0.73）mOD/(min?μg)]교정상대조조[분별위（0.57±0.06）μOD/（min?μg、（8.74±1.57）μOD/(min?μg)、（0.43±0.02）mOD/(min?μg)、（0.69±0.02）mOD/(min?μg)、（0.65±0.02）、（0.51±0.01）、（7.41±1.28）]강저（P＜0.01）；여모형조비교，지황음자가현저개선AD소서학습기억능력，제고뇌EC치、호흡련복합물I화IV활성、Na＋-K＋ATP매、Ca2＋ATP매활성여선립체막전위[분별위（0.57±0.07）、（8.42±1.74）μOD/(min?μg)、（0.64±0.03）mOD/(min?μg)、（0.68±0.04）、（0.55±0.01）、（6.69±1.03），（P＜0.01혹0.05）]。결론지황음자통과보호선립체，제고AD소서뇌능량대사，개선학습기억능력。
Objective To investigate the effects of Dihuang-Yinzi on cognition and energy metabolism of AD (Alzheimer’s disease) mice. Methods 60 Male APPsw/PS1ΔE9 mice were divided into 5 groups model, positive drug (Aricept), high, medium and low dosage of Dihuang-Yinzi. C57BL/6J mice with same age were served as normal control. All groups were orally administrated for 150 days. The spatial memory and passive avoidance were measured. The energy charge, activity of complex I, II and IV of respiratory chain, enzymatic activity of ATPase and mitochondrial membrane potential were assayed. Results APPsw/PS1ΔE9 mice showed significant impairments in cognition and energy production [(0.39±0.02),(3.28± 0.37)μOD/(min?μg),(0.19±0.04)mOD/(min?μg),(0.26±0.03)mOD/(min?μg),(0.19±0.02),(0.30±0.03)、(3.49±0.73)]with compaired to normal control[(0.57±0.06),(8.74±1.57)μOD/(min?μg),(0.43± 0.02)mOD/(min?μg),(0.69±0.02)mOD/(min?μg),(0.65±0.02),(0.51±0.01),(7.41±1.28)]. Dihuang-Yinzi ameliorates cognition decline, promotes acitivity of energy production related enyzmes, and restores mitochondrial membrane potential in AD mice[(0.57 ± 0.07),(8.42 ± 1.74)μOD/(min ?μg),(0.64 ± 0.03)mOD/(min?μg),(0.68±0.04),(0.55±0.01),(6.69±1.03), P<0.01 or 0.05]. Conclusion Dihuang-Yinzi could improve cognition and energy metabolism of APPsw/PS1ΔE9 mice by protecting mitochondria from pathologic injury.