• 동의신경정신과학회지
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• 제13권2호
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• pp.173-194
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• 2002

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the future AD will be the largest problem in public health service. From old times, Much medicines have been used for treatment of dementia, but there is no medicine having obvious effect. AD is one of brain retrogression disease. So We studied on herbal medicine that have a relation of brain retrogression. From old times, In Oriental Medicine, Rhizoma Acori Graminei has been used for disease in relation to brain retrogression. We studied on the effects of anti-Alzheimer in pCT105-induced neuroblastoma cell lines by Rhizoma Acori Graminei extract As the result of this study, In RAG group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of Neuroblastoma cells by CT105 expression is promoted. These results indicate that RAG possess strong inhibitory effect of apoptosis in the nervous system and repair effect against the degeneration of Neuroblastoma cells by CT105 expression.

• 대한한방내과학회지
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• 제27권3호
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• pp.603-616
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• 2006

The water extract of Gamiyaengshinhwan (GYH), has been used in vitro tests for its beneficial effects on neuronal survival and neuroprotective functions, particularly in connection with CT105-related dementias and Alzheimer's disease(AD). CT105 derived from proteolytic processing of the $\beta$-amyloid precursor protein (APP), including the amyloid-$\beta$ peptide ($A{\beta}$), plays a critical role in the pathogenesis of Alzheimer's dementia. We determined that transfected overexpressing APP695 and $A{\beta}$ CT105 have a profound attenuation in the Increase in CT105 expressing neuro2A cells from GYH. Experimental evidence indicates that GYH protects against neuronal damage from cells, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing CT105-associated neuronal degeneration, we demonstrated that GYH inhibits formation of amyloid-$\beta$ fragment ($A{\beta}$ CT105). which are the characteristic, and possibly causative, features of AD. The decreased CT105 $A{\beta}$ in the presence of GYH was observed in the conditioned medium of this CT105-secreting cell line under in vitro. In the cells, GYH significantly attenuated mitochondrion-initiated apoptosis and decreased the activity of Bax, a key enzyme in the apoptosis cell-signaling cascade. These results suggest that neuronal damage in AD might be due to two factors: a direct CT05 toxicity and the apoptosis initiated by the mitochondria. Multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of CT105 aggregation, underlie the neuroprotective effects of GYH.

• 동의생리병리학회지
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• 제17권4호
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• pp.1037-1049
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• 2003

Numerous lines of evidence indicate that some of the neurotoxicity associated with Alzheimer's disease (AD) is due to proteolytic fragments of the amyloid precursor protein (APP). Most research has focused on the amyloid 6 (M). However, the possible role of other cleaved products of APP is less clear. Lately It has been reported that a recombinant carboxy-terminal 105 amino acid fragment (CT105) of APP induced strong nonselective inward currents in Xenopus oocyte. In a brain with Alzheimer's disease (AD), to investigate the roles of carboxyl-terminal fragment (CT105) of amyloid precursor protein (APP) in apoptosis processes possibly linked to neurodegeneration associated with AD, we examined the effects of the CT of APP with 105 amino acid residues (CT105) on the alteration of apoptosis triggers in neubroblastoma cells. We have investigated whether Radix Polygalae and Rhizoma Acori Graminei mixture extract (RP+RAG) inhibits CT105-induced apoptosis of neuroblastoma cells. We found that RP+RAG inhibits CT105-induced apoptosis in SK-N-SH cells. Treatment of the cells with RP+RAG inhibited CT105-induced DNA fragmentation and Tunel assay of nuclear chromatin and inhibited the caspase-3 expression in SK-N-SH cells. As the result of this study, In RP+RAG group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of neuroblastoma cells by CT105 expression is promoted. These results indicate that RP+RAG possess strong inhibitory effect of apoptosis in the nervous system and repair effect against the degeneration of neuroblastoma cells by CT105 expression

• Journal of Ginseng Research
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• 제36권4호
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• pp.342-353
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• 2012

Ginseng, the root of the Panax ginseng, has been a popular and widely-used traditional herbal medicine in Korea, China, and Japan for thousands of years. Now it has become popular as a functional health food and is used globally as a natural medicine. Evidence is accumulating in the literature on the physiological and pharmacological effects of P. ginseng on neurodegenerative diseases. Possible ginseng- or ginsenosides-mediated neuroprotective mechanisms mainly involve maintaining homeostasis, and anti-inflammatory, anti-oxidant, anti-apoptotic, and immune-stimulatory activities. This review considers publications dealing with the various actions of P. ginseng that are indicative of possible neurotherapeutic efficacies in neurodegenerative diseases and neurological disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis and multiple sclerosis.

• Fisheries and Aquatic Sciences
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• 제22권5호
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• pp.10.1-10.14
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• 2019

Fish skin waste accounts for part of the solid waste generated from seafood processing. Utilization of fish skin by bioconversion into high-grade products would potentially reduce pollution and economic cost associated with treating fish processing waste. Fish skin is an abundant supply of gelatin and collagen which can be hydrolyzed to produce bioactive peptides of 2-20 amino acid sequences. Bioactivity of peptides purified from fish skin includes a range of activities such as antihypertensive, anti-oxidative, antimicrobial, neuroprotection, antihyperglycemic, and anti-aging. Fish skin acts as a physical barrier and chemical barrier through antimicrobial peptide innate immune action and other functional peptides. Small peptides have been demonstrated to possess biological activities which are based on their amino acid composition and sequence. Fish skin-derived peptides contain a high content of hydrophobic amino acids which contribute to the antioxidant and angiotensin-converting enzyme inhibitory activity. The peptide-specific composition and sequence discussed in this review can be potentially utilized in the development of pharmaceutical and nutraceutical products.

• Journal of Applied Biological Chemistry
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• 제64권3호
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• pp.299-307
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• 2021

뇌 내 amyloid beta (Aβ) 축적으로 인한 신경독성은 산화적 스트레스를 야기하여 알츠하이머 질환(Alzheimer's disease, AD)을 유도하는 것으로 알려져 있다. 본 연구는 여주(Momordica charantia L.)의 활성분획물인 butanol (BuOH) 분획물의 Aβ_25-35 유도 AD 동물모델에서 인지능 개선 효과에 대해 연구하였다. T-미로 실험 및 물체인지실험을 통해서 여주 BuOH 분획물 100 및 200 mg/kg/day 농도 투여군은 AD를 유도한 control군에 비해 유의적으로 새로운 경로와 물체를 탐색하는 비율이 감소되어 공간인지 및 물체인지능력 개선 효과를 확인하였다. 수중미로실험을 통해 학습·기억력에 미치는 효과를 측정한 결과, 여주 BuOH 분획물 투여군은 훈련을 반복할수록 숨겨진 도피대를 찾아가는 시간이 감소함을 통해 학습·기억력 개선 효과를 나타내었다. 여주 BuOH 분획물이 산화적 스트레스 개선 효과에 미치는 효과를 확인하기 위해 뇌, 간, 신장 조직에서 지질과 산화 함량 및 nitric oxideNO 생성량을 측정하였다. 여주 BuOH 분획물을 처리한 군은 Aβ_25-35를 주입한 control군에 비해 유의적으로 뇌, 간, 신장 조직에서 지질과산화 함량 및 NO 생성량이 감소되어 산화적 스트레스 개선 효과를 확인하였다. 따라서 본 연구는 여주 BuOH 분획물이 Aβ_25-35 유도 AD 동물모델에서 산화적 스트레스 개선을 통해 인지능력 개선 효과를 나타냄을 확인하였으며, 이에 따라 여주는 AD 예방 및 개선용 소재로써의 가능성이 있는 것으로 사료된다.

• 한국식품과학회지
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• 제38권3호
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• pp.452-455
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• 2006

퇴행성뇌질환인 치매의 정확한 원인은 아직 불분명하나 빠른 뇌세포사멸이 주요한 원인으로 알려져 있다. 특히, 알츠하이머형 치매는 다량 생성되는 활성산소에 의한 뇌세포사멸이 주요원인인 것으로 입증되고 있다. 따라서 본 연구에서는 웅담활성성분인 UDCA의 세포보호 및 항산화효과로부터 알츠하이머형 치매와 같은 퇴행성 뇌질환억제 또는 치료물질로서의 가능성을 입증하고자 하였고 뇌의 대식세포인 소교세포(microglia)를 cell model로 하였다. MTT 실험결과 UDCA에 의한 세포보호효과는 $7.5\;{\mu}g/mL$ 주변 농도에서 관찰되었고 NO에 의한 세포손상 유도억제효과를 확인하였다(Fig. 2). 이와 같은 결과는 형광현미경하에서 보다 명확히 관찰되어(Fig. 3) 결국 UDCA에 의한 항세포사효과가 있음을 알 수 있었다. UDCA의 항산효과는 활성산소인 $H_2O_2$의 단백질 분해 저해능을 관찰하는 금속이온촉매 산화효과를 통해 확인하였다(Fig. 4). 즉, UDCA는 농도의존적으로$(1{\sim}100\;{\mu}g/mL)$ 단백질 분해억제능을 보였으며 $100\;{\mu}g/mL$ 이상의 농도에서 양성대조군인 ascorbic acid와 유사한 억제효과를 나타냈다. 이와 같은 UDCA의 항산화효과는 $10\;{\mu}g/mL$ 전후에서 관찰되어 세포보호효과를 나타내는 농도$(7.5\;{\mu}g/mL)$와 큰 차이가 없는 것으로 사료되었고 따라서 UDCA의 농도범주는 일괄적 적용이 가능할 것으로 판단된다. 결론적으로 웅담활성성분인 UDCA는 일반적으로 사용하여온 간질환 및 소화계질환의 보조요법제의 개념을 벗어나 항염 및 항산화효과에 잠재능을 가지며 나아가 뇌신경세포를 보호하고 세포사를 차단하여 알츠하이머와 같은 퇴행성뇌질환 조절 후보물질로 적용이 가능할 것으로 판단되나 보다 심도 있는 in vivo 및 임상적 차원의 연구가 요구된다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.94-94
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• 2002

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimer's disease (AD). Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.327.2-327.2
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• 2002

Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of Alzheimer's disease (AD), and nonsteroidal anti-inflammatory drugs have been shown to retard the progress of AD. In this study, we have investigated the molecular mechanisms underlying oxidative and inflammatory cell death induced by beta-amyloid (Abeta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD, in cultured PC12 cells. (omitted)

• 대한의생명과학회지
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• 제27권4호
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• pp.248-254
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• 2021

Ulcerative colitis (UC), chronic inflammatory bowel disease, is characterized by severe inflammation in the colon. Tea is one of the most popular beverages consumed worldwide. Pu-erh tea, a unique Chinese tea produced by microbial activities, possesses a broad range of health-promoting effects, including anti-aging, anti-Alzheimer's disease, antioxidation and anti-obesity. However, the inhibitory effect of Pu-erh tea on intestinal inflammation and the underlying mechanism remain unclear. The present study was designed to evaluate the regulatory effect of Pu-erh tea extract (PTE) on dextran sulfate sodium (DSS)-induced colitis clinical signs by analyzing the weight loss and colon length in mice. The inhibitory effects of PTE on inflammatory mediators, such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, and the activation of nuclear factor-κB (NF-κB) were also determined in DSS-treated colitis tissue. We observed that PTE treatment significantly inhibited the DSS-induced clinical symptoms of weight loss, decrease,in colon length, and colon tissue damage in mice. Moreover, PTE attenuated the DSS-induced levels of IL-6 and TNF-α in colon tissue. We also demonstrated the anti-inflammatory mechanism of PTE by suppressing the activation of NF-κB in DSS-treated colon tissues. Collectively, the findings provide experimental evidence that PTE may be effective in preventing and treatment of intestinal inflammatory disorders, including UC.