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결명자 에탄올 추출물이 알코올로 유도로 유도한 기억 장애에 미치는 영향
권희영(Huiyoung Kwon),조은비(Eunbi Cho),전지은(Jieun Jeon),이영춘(Young Choon Lee),김동현(Dong Hyun Kim) 한국생명과학회 2019 생명과학회지 Vol.29 No.5
최근 알코올 소비량이 증가함에 따라 과량의 에탄올을 섭취하는 경우 또한 늘어나고 있다. 이런 과도한 에탄올 섭취는 γ-aminobutyric acid (GABA) 수용체의 활성화와 glutamate 수용체의 활성 억제를 통해 신경계를 교란시켜 단기 기억 형성을 방해 한다. 알코올에 의한 인지기능의 저하는 알코올성 black out을 유도할 수 있으며, 반복될 경우 알코올성 치매로 이어질 수 있기 때문에 black out을 예방하는 치료제의 개발이 필요하다. 따라서 본 연구자는 해당 연구를 통하여 Cassia obtusifolia seeds 에탄올 추출물(COE)이 가진 black out 예방제로써의 가능성을 평가하였다. 본 연구에서는 에탄올에 의해 유도된 기억 장애에 대한 COE의 효과를 확인하였다. 실험 동물의 기억력을 측정하기 위하여 수동 회피 실험과 Y자 미로 실험을 수행하였고, 마우스 해마 절편을 사용하여 에탄올이 기억의 형성과 관련하여 장기 강화(long term potentiation; LTP)에 어떠한 영향을 끼치는지 전기생리학을 통해 확인하였다. 또한 α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 수용체 길항제인 NBQX (50 μM)를 사용하여 에탄올에 의한 인지기능 장애와 관련이 있다고 알려진 N-Methyl-D-aspartate (NMDA) 매개 field 흥분성 시냅스 후 전위를 측정하였다. 결과적으로, COE는 에탄올에 의한 기억력의 손상을 방지하였고, 해마 절편에서 에탄올에 의해 감소된 LTP와 NMDA 매개 흥분성 시냅스 후 전위를 대조군과 비슷한 수준까지 회복시켰다. Heavy drinking disrupts the nervous system by activation of GABA receptors and inhibition of glutamate receptors, thereby preventing short-term memory formation. Degradation of cognition by alcohol induces blackouts, and it can lead to alcoholic dementia if repeated. Therefore, drugs need to be developed to prevent alcohol-induced blackout. In this study, we confirmed the effect of an ethanol extract of Cassia obtusifolia seeds (COE) on alcohol-induced memory impairment. The effects of COE and ethanol on cognitive functions mice were examined using the passive avoidance and Y-maze tests. The manner in which alcohol affects long-term potentiation (LTP) in relation to the learning and memory was confirmed by electrophysiology performed on mouse hippocampal slices. We also measured N-methyl-D-aspartate (NMDA) receptor-mediated field excitatory synapses (fEPSPs), which have a known association with cognitive impairment caused by ethanol. Ethanol caused memory impairments in passive avoidance and Y-maze tests. COE prevented these ethanol-induced memory impairments in these tests. Ethanol also blocked LTP induction in the mouse hippocampus, and COE prevented this ethanol-induced LTP deficit. Ethanol decreased NMDA receptor-mediated fEPSPs in the mouse hippocampus, and this decrease was prevented by COE. These results suggest that COE might be useful in preventing alcohol-induced neurological dysfunctions, including blackouts.
Lee, Jihye,Kwon, Huiyoung,Yu, Jimin,Cho, Eunbi,Jeon, Jieun,Lee, Seungheon,Ryu, Jong Hoon,Lee, Young Choon,Kim, Dong Hyun,Jung, Ji Wook Elsevier 2018 Journal of Ethnopharmacology Vol.224 No.-
<P><B>Abstract</B></P> <P><B>Ethnopharmacological relevance</B></P> <P>Aubang Gahl Soo (AGS) is a Korean traditional drink manufactured from medicinal plants and fruits using sugar or honey. Although traditional old book stated its effects on body, there is no scientific evidence yet. Therefore, in the present study, we tested AGS on brain functions.</P> <P><B>Aim of this study</B></P> <P>In this study, we tried to uncover the effect of on brain functions. To do this we examined the action of AGS on the hippocampal synaptic function and memory in mice.</P> <P><B>Materials and methods</B></P> <P>To examine the effect of AGS on synaptic plasticity, we observed input-output curves (I/O curve), paired-pulse facilitation (PPF), and long-term potentiation (LTP) using mouse hippocampal slices. Moreover, to investigate the functional relevance of the effect of AGS on synaptic plasticity, we conducted passive avoidance, Y-maze and Morris water maze tests. To examine relevant mechanism, acetylcholinesterase (AChE) activity and acetylcholine (ACh) level assay were also conducted.</P> <P><B>Results</B></P> <P>In the basal synaptic transmission study, we found that AGS did not affect I/O curves and PPF. However, AGS facilitated hippocampal LTP in a concentration-dependent manner. Moreover, AGS blocked AChE activity (IC<SUB>50</SUB> = 485 μg/ml). Moreover, ACh level was increased by AGS (100 μg/ml) treatment. Along with this, facilitating effect of AGS on hippocampal LTP also blocked by scopolamine, a muscarinic acetylcholine receptor antagonist. Moreover, AGS also ameliorated memory impairments induced by scopolamine in passive avoidance, Y-maze, and Morris water maze tests.</P> <P><B>Conclusions</B></P> <P>These results suggest that AGS facilitates hippocampal LTP through activating cholinergic system and ameliorates cholinergic dysfunction-induced memory deficit.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
( Mudan Cai ),( Inho Jung ),( Huiyoung Kwon ),( Eunbi Cho ),( Jieun Jeon ),( Jeanho Yun ),( Young Choon Lee ),( Dong Hyun Kim ),( Jong Hoon Ryu ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.2
Hippocampal synaptic dysfunction is a hallmark of Alzheimer’s disease (AD). Many agents regulating hippocampal synaptic plasticity show an ameliorative effect on AD pathology, making them potential candidates for AD therapy. In the present study, we investigated spinosin as a regulating agent of synaptic plasticity in AD. Spinosin attenuated amyloid β (Aβ)-induced long-term potentiation (LTP) impairment, and improved plasmin activity and protein level in the hippocampi of 5XFAD mice, a transgenic AD mouse model. Moreover, the effect of spinosin on hippocampal LTP in 5XFAD mice was prevented by 6-aminocaproic acid, a plasmin inhibitor. These results suggest that spinosin improves synaptic function in the AD hippocampus by regulating plasmin activity.
β-Amyrin Ameliorates Alzheimer’s Disease-Like Aberrant Synaptic Plasticity in the Mouse Hippocampus
( Hye Jin Park ),( Huiyoung Kwon ),( Ji Hye Lee ),( Eunbi Cho ),( Young Choon Lee ),( Minho Moon ),( Mira Jun ),( Dong Hyun Kim ),( Ji Wook Jung ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.1
Alzheimer’s disease (AD) is a progressive and most frequently diagnosed neurodegenerative disorder. However, there is still no drug preventing the progress of this disorder. β-Amyrin, an ingredient of the surface wax of tomato fruit and dandelion coffee, is previously reported to ameliorate memory impairment induced by cholinergic dysfunction. Therefore, we tested whether β-amyrin can prevent AD-like pathology. β-Amyrin blocked amyloid β (Aβ)-induced long-term potentiation (LTP) impairment in the hippocampal slices. Moreover, β-amyrin improved Aβ-induced suppression of phosphatidylinositol-3-kinase (PI3K)/Akt signaling. LY294002, a PI3K inhibitor, blocked the effect of β-amyrin on Aβ-induced LTP impairment. In in vivo experiments, we observed that β-amyrin ameliorated object recognition memory deficit in Aβ-injected AD mice model. Moreover, neurogenesis impairments induced by Aβ was improved by β-amyrin treatment. Taken together, β-amyrin might be a good candidate of treatment or supplement for AD patients.
Park, Hye Jin,Jung, In Ho,Kwon, Huiyoung,Yu, Jimin,Jo, Eunbi,Kim, Haneul,Park, Se Jin,Lee, Young Choon,Kim, Dong Hyun,Ryu, Jong Hoon Elsevier Ireland Ltd 2019 Journal of Ethnopharmacology Vol.233 No.-
<P><B>Abstract</B></P> <P><B>Ethnopharmacological relevance</B></P> <P>The seeds of Zizyphus jujuba var. spinosa (Bunge) Hu ex H.F. Chow (Rhamnaceae) have long been treated as hypnotic agent for sleep disturbances in traditional Chinese and Korean medicine and many previous studies have focused on its effect in central nervous system.</P> <P><B>Aims of study</B></P> <P>The present study aimed to provide evidence showing that the ethanol extract of <I>Zizyphus jujuba</I> var. <I>spinosa</I> seeds (EEZS), which may regulate plasmin activity, has the potential to serve as a therapeutic agent for AD.</P> <P><B>Materials and methods</B></P> <P>Synaptic function was determined by measuring long-term potentiation (LTP) in Shaffer-collateral pathway of the hippocampus. Protein levels of plasmin or plasminogen were examined using western blotting. Plasmin activity was measured using ELISA. Cognitive functions were measured using passive avoidance and object recognition tests in the 5XFAD mice.</P> <P><B>Results</B></P> <P>Our <I>in vitro</I> analysis revealed that EEZS-treated hippocampal slices from 5XFAD mice, a mouse model of AD, showed significantly higher long-term potentiation levels than did vehicle-treated hippocampal slices from 5XFAD mice (<I>P</I> < 0.05). Additionally, EEZS significantly elevated the plasmin level and activity in the hippocampal slices from 5XFAD mice (<I>P</I> < 0.05). Co-treating the slices with EEZS and 6-aminocaproic acid, a plasmin inhibitor, blocked the ameliorating effects of EEZS on the synaptic deficits that were present in 5XFAD mice. Compatible with the <I>in vitro</I> study, the results of our <I>in vivo</I> investigation showed that administering EEZS orally to 5XFAD mice ameliorated their memory impairments. Orally administered EEZS also elevated the plasmin level and activity in the hippocampus of 5XFAD mice.</P> <P><B>Conclusions</B></P> <P>Collectively, our findings suggest that EEZS alleviates the AD-like symptoms in 5XFAD mice by regulating of plasmin activity and EEZS may be a suitable treatment for AD.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>