• Journal of Acupuncture Research
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• 제23권2호
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• pp.33-46
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• 2006

Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease associated with aging in the human population. This disease is characterized by the extracellular deposition of beta-amyloid peptide $(A{\beta})$ in cerebral plaques. $A{\beta}$ is derived from the ${\beta}-amyloid$ precursor protein (APP) by the enzymes, ${\beta}-$ and ${\eta}o-secretase$. Compounds that ${\beta}-$ or ${\eta}o-secretase$ inhibit activity, can reduce the production of $A{\beta}$ peptides, and thus have therapeutic potential in the treatment of AD. Increasing body of evidence has been demonstrated that Bee Venom(BV) Acupuncture could compete with complex protein involving in multiple step of $NF-{\kappa}B$ activation and exert the anti-inflammatory potential of combined inhibition of the prostanoid and nitric oxide synthesis systems by inhibition of IKK and $NF-{\kappa}B$. In this study, I investigated possible effects of BV on memory dysfunction caused by lipopolysaccharide (LPS) and $A{\beta}$ through inhibition of secretases activities and $A{\beta}$ aggregation. I examined the improving effect of BV on the LPS (2.5 mg/Kg, i.p.)-induced memory dysfunction using passive avoidance response and water maze tests in the mice. BV (0.84, $1.67\;{\mu}g/ml$) reversed the LPS-induced memorial dysfunction in dose dependent manner. BV also dose-dependently attenuated LPS-induced ${\beta}$ and ${\eta}o-secretase$ activities in cerebral cortex and hippocampus of the mice brain. This study therefore suggests that BV acupuncture method may be useful for prevention of development or progression of AD.

• 전자공학회논문지CI
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• 제45권1호
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• pp.55-61
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• 2008

실시간 삼차원 영상은 충돌 방지를 위한 수동 시스템을 포함하는 다양한 응용 분야에 활용될 수 있으며, 기존 능동 시스템에 대한 훌륭한 대안으로서 잡음이 많은 복잡한 환경에서 외부의 영향을 최소화 할 수 있는 장점이 있다. 본 논문에서는 하드웨어 자원 사용량에 주목하여 실시간 삼차원 영상을 위한 스테레오 비전 시스템의 최적화에 관한 연구를 진행하였다. SAD 알고리즘은 규칙적인 구조, 선형적인 데이터 흐름과 풍부한 병렬성을 가지므로 재구성 가능한 하드웨어에서 구현하기 위한 좋은 조건을 가지고 있다. HDL을 이용하여 SAD 정합연산기를 설계하고 하드웨어 자원 사용량과 성능을 확인하기 위해서 Xilinx를 사용하여 합성하였다. 실험을 통하여, 초당 30프레임을 실시간으로 처리할 수 있는 충분한 처리 속도를 가지고 있으며, 적은 자원은 사용하면서 높은 정합율을 보이는 SAD 정합연산기를 설계하였음을 확인하였다.

• Animal cells and systems
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• 제16권4호
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• pp.302-312
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• 2012

The purpose of this study was to examine whether Phellodendri Cortex extract (PCE) could improve learning and memory impairments caused by lipopolysaccharide (LPS)-induced inflammation in the rat brain. The effect of PCE on modulating pro-inflammatory mediators in the hippocampus and its underlying mechanism were investigated. Injection of LPS into the lateral ventricle caused acute regional inflammation and subsequent deficits in spatial learning ability in the rats. Daily administration of PCE (50, 100, and 200 mg/kg, i.p.) for 21 days markedly improved the LPS-induced learning and memory disabilities in the Morris water maze and passive avoidance test. PCE administration significantly decreased the expression of pro-inflammatory mediators such as tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$, and cyclooxygenase-2 mRNA in the hippocampus, as assessed by RT-PCR analysis and immunohistochemistry. Together, these findings suggest that PCE significantly attenuated LPS-induced spatial cognitive impairment through inhibiting the expression of pro-inflammatory mediators in the rat brain. These results suggested that PCE may be effective in preventing or slowing the development of neurological disorders, including Alzheimer's disease, by improving cognitive and memory function because of its anti-inflammation activity in the brain.

• 한국약용작물학회지
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• 제17권6호
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• pp.388-396
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• 2009

The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid $\beta$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to $10\;{\mu}M$ $A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $1-50\;{\mu}g/m{\ell}$, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with HS0608 (25, 50 and 100 mg/kg, p.o. for 7 days) as measured by a passive avoidance test. From these results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer's disease.

• Journal of Korean Biological Nursing Science
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• 제19권4호
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• pp.276-283
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• 2017

Purpose: The aim of this study was to identify the effects of environmental factors on depressive-like behavior and memory function during adolescence. We performed behavior tests in adolescent rats exposed to environmental enrichment, handling, and social deprivation for eight weeks. Methods: Wistar rats were randomly assigned to control, environmental enrichment, handling, and social deprivation groups at the age of four weeks. Results: In the forced swim test, the immobility time in the environmental enrichment group was decreased than that in the control group (p=.038), while the immobility time in the social deprivation group was increased than that in the control group (p=.035), the environmental enrichment group (p<.001), and the handling group (p=.001). In the Morris water maze test, the social deprivation group had an increased latency time than the control group (p=.013) and the environmental enrichment group (p=.001). In the passive avoidance test, the environmental enrichment group had an increased latency time than the control group (p=.005). However, the social deprivation group had reduced latency time than the socially housed groups (control: p=.030; environmental enrichment: p<.001; handling: p<.001). Conclusion: These findings suggest that environmental factors play an important role in emotion and memory function during adolescence.

• The Korean Journal of Physiology and Pharmacology
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• 제22권3호
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• pp.257-267
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• 2018

The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30-35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p.), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p.). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice.

• 한국약용작물학회지
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• 제20권1호
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• pp.8-15
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• 2012

The present study investigated an ethanol extract of Chaenomeles sinensis fruit (CSF) for possible neuroprotective effects on neurotoxicity induced by amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and also for antidementia activity in mice. Exposure of cultured cortical neurons to $10{\mu}M\;A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $0.1-10{\mu}g/m{\ell}$, CSF inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of mice with 15 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with CSF (10, 25 and 50 mg/kg, p.o. for 7 days) as measured by a passive avoidance test. CSF (50 mg/kg) inhibited the increase of cholinesterase activity in $A{\beta}$ (25-35)-injected mice brain. From these results, we suggest that the antidementia effect of CSF is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that CSF may have a therapeutic role for preventing the progression of Alzheimer's disease.

• 대한교통학회지
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• 제33권6호
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• pp.509-519
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• 2015

최근 사업용운전자들의 음주운전이 증가하고 있다. 본 연구는 사업용운전자들의 음주문제행동에 영향을 미치는 요인으로 스트레스 대처방식을 상정하고 스트레스 대처방식이 생활스트레스를 증가시켜 음주문제행동에 영향을 주는지를 알아보고자 하였다. 총 1308명의 사업용운전자들이 연구에 참여하였다. 연구결과, 사업용운전자들의 스트레스 대처방식으로 문제해결, 조력추구, 정서적 완화, 소망적 사고, 수동적 회피 5개 방식이 확인되었으며, 이 중 문제해결, 소망적 사고, 수동적 회피 대처방식에서만 생활스트레스의 매개효과가 관찰되었다. 즉 문제해결 전략을 적게 사용할수록, 소망적 사고와 수동적 회피 전략을 많이 사용할수록 생활스트레스는 높았으며, 이것은 다시 음주문제행동을 높이는 것으로 나타났다. 이러한 결과는 스트레스 대처방식에 대한 운전자 교육의 필요성을 시사하고 있다.

• 한국약용작물학회지
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• 제25권6호
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• pp.353-360
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• 2017

Background: A critical features of Alzheimer's disease (AD) is cognitive dysfunction, which partly arises from decreased in acetylcholine levels. AD afftected brains are characterized by extensive oxidative stress, which is thought to be primarily induced by the amyloid beta ($A{\beta}$) peptide. In a previous study, Cinnamomum loureiroi tincture inhibited acetylcholinesterase (AchE) activity. That study identified AChE inhibitor in the C. loureiroi extract. Furthermore, the C. loureiroi extract enhanced memory in a trimethyltin (TMT)-induced model of cognitive dysfunction, as assessed via two behavioral tests. Rosa laevigata extract protected against oxidative stress-induced cytotoxicity. Administrating R. laevigata extracts to mice significantly reversed $A{\beta}$-induced learning and memory impairment, as shown in behavioral tests. Methods and Results: We conducted behavioral to examine the synergistic effects of C. loureiroi and R. laevigata extracts in inhibiting AChE and counteracting TMT-induced learning and memory losses. We also performed biochemical assays. The biochemical results showed a relationship between increased oxidative stress and cholinergic neurons damage in TMT-treated mice. Conclusions: A diet containing C. loureiroi and R. laevigata extracts ameliorated learning and memory impairments in the Y-maze and passive avoidance tests, and exerted synergistic inhibitory effect against AChE and lipid peroxidation.

• Biomolecules & Therapeutics
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• 제25권3호
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• pp.249-258
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• 2017

To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a naïve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-${\zeta}$ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-${\zeta}$ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.