• 한국응용과학기술학회지
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• 제35권2호
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• pp.389-398
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• 2018

본 연구는 노루궁뎅이버섯 균사체로 발효시킨 엄나무 추출물의 항산화 및 항아밀로이드 활성을 알아보고자 하였다. 항산화 활성은 2,2-diphenyl-1-picrylhydrazyl(DPPH) radical, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)(ABTS) radical 소거 측정법을 사용하여 관찰하였다. 엄나무추출물(KP), 노루궁뎅이버섯 균사체 추출물(HE), 엄나무 발효물(KP-HE)에서 모두 라디칼 소거활성이 관찰되었다. 그러나 KP-HE가 KP와 HE에 비해서 더 높은 소거 활성을 갖는 것으로 관찰되었다. KP-HE는 peroxyl radical에 의한 DNA의 산화적 손상을 억제하였다. 알츠하이머병 (Alzheimer's disease: AD)과 관련 있는 $A{\beta}_{1-42}$의 응집에 KP, HE, KP-HE가 어떤 영향을 미치는 지를 알아보았다. KP와 HE는 $A{\beta}_{1-42}$의 응집에 거의 영향을 미치지 않았고 KP-HE는 $A{\beta}_{1-42}$의 응집을 효과적으로 억제하였다. 또한 $A{\beta}_{1-42}$에 의한 신경세포 사멸에 엄나무 발효물을 $300{\mu}g/mL$ 농도로 전 처리한 세포생존율은 20.3% 높게 증가되었다. 또한 엄나무 발효물을 $50{\mu}g/mL$ 농도로 처리했을 경우 세포 내 ROS의 축적이 유의적으로 감소되었다. 결론적으로 본 연구에서 관찰된 결과들을 통해 엄나무 발효물은 항산화 및 항아밀로이드 활성을 가지는 것으로 확인되었다. 따라서 엄나무 발효물은 알츠하이머병과 같은 퇴행성 뇌질환을 예방할 수 있는 식품소재로 이용될 수 있을 것으로 사료된다.

• 대한본초학회지
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• 제34권3호
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• pp.1-7
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• 2019

Objectives : Amyloid ${\beta}(A{\beta})$ could induce cognitive deficits through oxidative stress, inflammation, and neuron death in Alzheimer's disease (AD). This study was investigated the effect of Angelica keiskei KOIDZUMI (AK) on memory in $A{\beta}$-induced an AD model. Methods : AK was extracted uses 70% ethanol solvent. Total polyphenol and flavonoids content were obtained by the Folin-Ciocalteu and the Ethylene glycol colorimetric methods, respectively. The antioxidant activities were assessed through free radical scavenging assays using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazolin-6-sulfonic acid) (ABTS) methods. Intracerebroventrical (i.c.v) injection of $A{\beta}$ 1-42 was used to induce AD in male ICR mice, followed by administrations of 5, 10 or 20 mg/kg AK on a daily. Animals were subjected to short and long term memory behavior in Y-maze and passive avoidance test. Results : The total polyphenol and flavonoids contents of the AK extract were $88.73{\pm}6.36mg$ gallic acid equivalent/g, $84.21{\pm}5.04mg$ rutin equivalent/g, respectively. The assays of DPPH and ABTS revealed that AK extract in treated concentrations (31.25, 62.5, 125, 250, 500, $1000{\mu}g/m{\ell}$) increased antioxidant activity in a dose-dependent manner. Oral administration of AK extract significantly reversed the $A{\beta}$ 1-42-induced decreasing of the spontaneous alternation in the Y-maze test and $A{\beta}$ 1-42-induced shorting of the step-through latency in the passive avoidance test. Conclusions : The findings suggest that AK indicated the antioxidant protective effects against $A{\beta}$-induced memory deficits, and therefore a potential lead natural therapeutic drug or agent for AD.

• 약학회지
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• 제56권5호
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• pp.293-298
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• 2012

The present study tested the effect of Schizandra chinensis lignan compounds, Gomisin A and Schizandrin, on the aggregation and dissociation of beta-amyloid $(A{\beta})_{1-42}$ to explore a possible therapeutic target for Alzheimer's disease. Gomisin A significantly inhibited the $A{\beta}_{1-42}$ aggregation in a dose dependent manner, but did not induced the dissociation of aggregated $A{\beta}_{1-42}$. On the other hand, Schizandrin significantly suppressed the aggregation and dissociation of $A{\beta}_{1-42}$. These results suggest that Gomisin A and Schizandrin, which are known as biologically active ingredients from Schizandra chinensis, may be potentially useful target molecules to develop a drug for the prevention or treatment of Alzheimer's disease.

• 한국균학회지
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• 제44권4호
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• pp.296-299
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• 2016

표고는 항암활성과 면역활성을 촉진하는 렌티난이라는 ${\beta}$-glucan을 가진 식용버섯이다. 본 연구에서는 표고 톱밥재배에서 배지의 영양원의 종류와 버섯 발생온도에 따른 표고조직의 ${\beta}$-glucan 함량의 변화를 메가자임법으로 조사하였다. 배지 중량이 감소하면서 버섯생산량은 증가하였지만, 이 생산량은 중량감소보다 영양원 종류에 더 크게 영향을 받았다. 콩비지 + $CaCl_2$ 처리구(50.4%)를 제외한 표고의 ${\beta}$-glucan 함량은 39.5~42.1% 범위였다. 자실체 발생 온도에 따른 ${\beta}$-glucan 함량은 발생온도 증가에 따라 반비례 관계가 나타났고, 저온 발생조건에서 42.4%였다.

• 생명과학회지
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• 제20권3호
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• pp.444-452
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• 2010

본 연구의 목적은 PS-2 (N141I) 알츠하이머 형질전환 모델 생쥐를 대상으로 트레드밀 운동이 뇌의 세포질과 미토콘드리아의 $A{\beta}$-42, cytochrome c, SOD-1, 2 and Sirt-3 단백질 발현에 미치는 효과를 알아보는데 있다. 우선 알츠하이머 형질전환 생쥐를 Non-Tg-sedentary (n=5), Non-Tg-treadmill exercise (n=5) 집단과 Tg-sedentary (n=5), Tg-treadmill exercise (n=5) 집단으로 구분하고 트레드밀 운동을 통한 신경보호 효과를 검증하기 위해 Tg와 Non-Tg집단에 12주간 트레드밀 운동을 수행한 후 인지능력을 살펴보고 뇌의 세포질과 미토콘드리아의 $A{\beta}$-42, cytochrome c, anti-oxidant enzymes (SOD-1, SOD-2)와 Sirt-3 단백질을 분석하였다. 먼저 트레드밀운동은 Tg 집단에서 인지능력의 개선을 나타냈으며 미토콘드리아의 $A{\beta}$-42와 세포질의 cytochrome c 단백질의 감소와 항산화 효소인 SOD-1, SOD-2를 유의하게 증가시켰다. 게다가 트레드밀 운동은 모든 집단에서 Sirt-3 단백질의 발현을 증가시켰다. 따라서 트레드밀 운동은 인지능력의 향상과 세포 내 스트레스를 유발하는 $A{\beta}$-42를 억제시켜 알츠하이머 질환을 개선시킬 수 있는 효과적인 방법이라고 생각된다.

• 한국컴퓨터정보학회논문지
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• 제25권6호
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• pp.165-170
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• 2020

본 논문에서는 스코폴레틴이 알츠하이머병 신경염증보호제로서의 가능성을 제안하기 위해 미세아교세포 BV-2에서 아밀로이드베타 올리고머(Aβ_1-42)로 유도된 염증을 억제하는지 확인하였다. 또한, 염증관련 사이토카인 및 염증매개인자가 어떠한 메커니즘으로 조절되는지 확인하였다. 알츠하이머병은 가장 흔한 신경 퇴행성 질환이지만, 특정 병인을 알 수 없는 질환이며, 이를 해결하기 위해 많은 연구에서 노력을 기울이고 있다. 우리는 먼저 스코폴레틴과 Aβ_1-42가 BV-2 세포에 독성을 보이는지 확인하기 위해 CCK-8 assay 방법으로 세포 생존율을 측정하였다. Western Blot을 통해 Aβ_1-42로 유도된 염증반응에서 interleukin 1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), nuclear factor-κB (NF-κB)의 발현정도를 분석하였다. ANOVA 분석법을 통해 Aβ_1-42를 단독 처리한 BV-2 세포와 스코폴레틴을 전 처리한 BV-2 세포에서 단백질 발현 차이를 비교하였다. 그 결과 스코폴레틴을 전 처리한 BV-2 세포에서 IL-1β, COX-2, iNOS, NF-κB 발현수준이 유의미하게 감소되었다 (p value < 0.05). 따라서 본 연구는 향후 스코폴레틴이 알츠하이머병의 신경염증보호제로서 개발 가치가 있음을 제시하였다.

• Journal of Ginseng Research
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• 제37권1호
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• pp.100-107
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• 2013

This study examined the effect of fermented ginseng (FG) on memory impairment and ${\beta}$-amyloid ($A{\beta}$) reduction in models of Alzheimer's disease (AD) in vitro and in vivo. FG extract was prepared by steaming and fermenting ginseng. In vitro assessment measured soluble $A{\beta}42$ levels in HeLa cells, which stably express the Swedish mutant form of amyloid precursor protein. After 8 h incubation with the FG extract, the level of soluble $A{\beta}42$ was reduced. For behavioral assessments, the passive avoidance test was used for the scopolamine-injected ICR mouse model, and the Morris water maze was used for a transgenic (TG) mouse model, which exhibits impaired memory function and increased $A{\beta}42$ level in the brain. FG extract was treated for 2 wk or 4 mo on ICR and TG mice, respectively. FG extract treatment resulted in a significant recovery of memory function in both animal models. Brain soluble $A{\beta}42$ levels measured from the cerebral cortex of TG mice were significantly reduced by the FG extract treatment. These findings suggest that FG extract can protect the brain from increased levels of $A{\beta}42$ protein, which results in enhanced behavioral memory function, thus, suggesting that FG extract may be an effective preventive or treatment for AD.

• Archives of Pharmacal Research
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• 제26권12호
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• pp.1067-1073
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• 2003

Ursodeoxycholic acid (UDCA) is a non-toxic, hydrophilic bile acid in widespread clinical use mainly for acute and chronic liver disease. Recently, treatment with UDCA in hepatic graft-versus-host disease has been given in immunosuppressive therapy for improvement of the biochemical markers of cholestasis. Moreover, it has been reported that UDCA possesses immunomodulatory effects by the suppression of cytokine production. In the present study, we hypothesized that UDCA may inhibit the production of the pro-inflammatory cytokine, IL-1$\beta$, and nitric oxide (NO) in microglia. In the study, we found that 100 $\mu$ g/mL UDCA effectively inhibited these two pro-inflammatory factors at 24 hand 48 h, compared to the $A\beta$42-pretreated groups. These results were compared with the LPS+UDCA group to confirm the UDCA effect. As microglia can be activated by several stimulants, such as $A\beta$42, in Alzheimers brain and can release those inflammatory factors, the ability to inhibit or at least decrease the production of IL-1$\beta$ and NO in Alzheimers disease (AD) is essential. Using RT-PCR, ELISA and the Griess Reagent System, we therefore found that UDCA in $A\beta$42 pre-treated cultures played a significant role in suppressing the expression or the production of IL-1$\beta$ and NO. Similarly, lipopolysaccharide (LPS) did not activate microglia in the presence of UDCA. Moreover, we found that UDCA exhibits a prolonged effect on microglial cells (up to 48 h), which suggests that UDCA may play an important role in chronic cell damage due to this long effect. These results further imply that UDCA could be an important cue in suppressing the microglial activation stimulated by massive AD peptides in the AD progressing brain.

• 한국수산과학회지
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• 제50권1호
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• pp.85-91
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• 2017

Alzheimer's disease (AD) is a progressive neurodegenerative disorder of insidious onset that causes gradual loss of memory and cognitive function, and it is the most common form of dementia in the elderly. AD is characterized by neuritic plaques and neurofibrillary tangles in the brain, together with loss of neuronal cells. The major neuropathological hallmark of AD is the accumulation of extracellular neurotoxic ${\beta}-amyloid$ ($A{\beta}$) peptides, such as $A{\beta}1-42$, in the brain. In the present study, we investigated the effect of sargachromenol (SCM), sargaquinoic acid (SQA) and sargahydroquinoic acid (SHQA) isolated from Sargassum serratifoilum ethanol extract (SSE) on $A{\beta}$ production in vitro using APP751-transfected Chinese hamster ovary cells (CHO-751). CHO-751 cells were treated with various concentrations of SSE, SCM, SQA and SHQA, and the level of extracellular $A{\beta}1-42$ was evaluated by enzyme-linked immunosorbent assay. SSE and SHQA reduced the production of $A{\beta}1-42$ in CHO-751 cells. Therefore, SHQA isolated from S. serratifolium has potential as an inhibitor of neurotoxic $A{\beta}$ peptide production.

• 생물정신의학
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• 제5권1호
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• pp.66-70
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• 1998

Apoptosis is a form of cell death in which the cells shrink and exhibit nuclear chromatin condensation and DNA fragmentation, and yet maintain membrane integrity. Many lines of evidence have shown that brain neurons are vulnerable to degeneration by apoptosis. Also it has been suggested that apoptosis is one of the mechanism contributing neuronal loss in Alzheimer's disease(AD), since the conditions in the disease($A{\beta}$ peptide, oxidative stress, low energy metabolism) are the inducers that activate apoptosis. Indeed some neurons in vulnerable regions of the AD brain show DNA damage, chromatin condensation, and apoptic bodies. Consistently, mutations in AD causative genes(Amyloid precursor protein, Presenilin-1 and Presenilin- 2) increase $A{\beta}$ $peptide_{1-42}(A{\beta}_{1-42})$ and sensitize neuronal cell to apoposis. However, several lines of evidence have shown that the location of neuronal loss and $A{\beta}$ peptide deposition is not correlated in AD brain and transgenic mice brain over-expressing $A{\beta}_{1-42}$. Taken together, these data may indicated that $A{\beta}$ peptide(and other causative factors of AD) can interact with other cellular insults or risk factors to exacerbate pathological mechansim of AD through apoptosis. Thus, this review discusses possible role and mechanism of apoptosis in AD.