• 대한한의정보학회지
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• 제19권2호
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• pp.1-20
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• 2013

This research observed the interrelations between the active components found specifically in red ginseng and fermented red ginseng from among the variety of ginseng variations and the protective effect and anti-oxidant effect exercised on brain cells in the animal model for MPTP-induced neurotoxic Parkinson's Disease and obtained the following conclusions. The results above comprehensively demonstrated that the fermented red ginseng extract exercised greater protective effects against oxidant brain damage by MPTP when compared to the group administered with the red ginseng extract. This was induced an increase in TH protein expression, and further raised the efficiency of the anti-oxidant enzyme defensive system against neurotoxicity, thereby restraining the lipid peroxidation caused by the active oxygen generated during the course of MPTP metabolism and enhancing the body's defensive capacities in response to tissue damage, thereby demonstrating a protective effect against MPTP induced neurotoxicity.

• BMB Reports
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• 제42권6호
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• pp.380-386
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• 2009

In neurodegenerative diseases, such as Alzheimer' and Parkinson', microglial cell activation is thought to contribute to CNS injury by producing neurotoxic compounds. Prothrombin and kringle-2 increase levels of NO and the mRNA expression of iNOS, IL-1$\beta$, and TNF-$\alpha$ in microglial cells. In contrast, the human prothrombin kringle-2 derived peptide NSA9 inhibits NO release and the production of pro-inflammatory cytokines such as IL-1$\beta$, TNF-$\alpha$, and IL-6 in LPS-activated EOC2 microglia. In this study, we investigated the anti-inflammatory effects of NSA9 in human prothrombin- and kringle-2-stimulated EOC2 microglia. Treatment with 20-100 ${\mu}M$ of NSA9 attenuated both prothrombin- and kringle-2-induced microglial activation. NO production induced by MAPKs and NF-$\kappa$B was similarly reduced by inhibitors of ERK (PD98059), p38 (SB203580), NF-$\kappa$B (N-acetylcysteine), and NSA9. These results suggest that NSA9 acts independently as an inhibitor of microglial activation and that its effects in EOC2 microglia are not influenced by the presence of kringle-2.

• 동의생리병리학회지
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• 제24권1호
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• pp.91-95
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• 2010

Alzheimer's disease (AD) is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of ${\beta}$-amyloid (A${\beta}$) peptides. It is urgent to develop effective therapies for the treatment of AD, since our society rapidly accelerate aging. A${\beta}$ peptides have been believed to be neurotoxic and now are also considered to have affects on the mechanism of memory formation, which are generated by processing of amyloid precursor protein (APP). In this study, effects of Styrax Liquides (SL) on the metabolism of APP were analyzed. SL inhibited the secretion of A${\beta}$ from the Neuro2a cell line (APPswe cell) expressing a mutation of APPswe. Immunoblotting study showed that it inhibited ${\beta}$-site APP cleaving enzyme (BACE) from the APPswe cells. We suggest that SL inhibits APP metabolism and A${\beta}$ generation by the means of BACE inhibitory mechanism. This is the first report that SL inhibits the secretion of A${\beta}$ peptides from neuroblastoma cells.

• 한국안광학회지
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• 제9권2호
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• pp.257-267
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• 2004

본 연구에서는 전라남도 여수지역의 한 석유화학단지애서 적어도 6개월이상 근무한 작업자 1030명을 대상으로 Lanthony D-15-desaturated 검사법을 이용하여 유기용제노출과 후천적 색각이상간의 연관성을 조사하였다. 작업환경측정은 전 작업시간(8시간) 단시료를 각 작업자에게 부착하는 개인시료를 활용하여 각 개인별 평균, 최대, 누적 연평균 8hr TWA를 산출하였다. 연구결과 연령이 높을수록 색혼란지수(CCI)가 유의하게 높았다(P<0.005). 형태에서는 청황색각이상의 분포가 노출군과 비노출군간에 통계적으로 유의한 수준은 아니었지만, 후천적 색각이상에서 주로 나타나는 제3색형과 제4색형 그리고 복합형이 대부분 노출군에서 높은 분포(비노출군 6.16%, 7.55%, 13.71%, 노출군 5.9%, 7.86%, 14.99%)를 보였다. 마지막으로 색각이상과 관련된 변수들을 보정하였을 때, 후천적 색각이상이 좌안에서는 비노출군과 비교하여 볼 때 통계적 연관성은 없었으나 노출군의 Odds ratio가 증가함을 보였다. 또한 연령에 대하여는 좌 우안에서 모두 높은 통계적 연관성을 보였다(p<0.01). 따라서 이 상의 결과로 근로자가 유기용제 중독으로 인해 초기 신경계이상의 증상으로 후천적 색각이상이 존재할 수 있으므로 안보건 사업에서의 또 하나의 일환으로 근로자의 안보건상태에 대한 지속적인 관심과 관리가 필요하다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권9호
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• pp.3901-3906
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• 2014

Aim: The purpose of this study was to investigate anti-tumor effects and safety of DH332, a new ${\beta}$-carboline alkaloids derivatives in vitro and in vivo. Materials and Methods: The effects of DH332 on human (RAMOS RA.1) and mouse (J558) B lymphoma cell lines were detected using a CCK-8 kit (Cell Counting Kit-8), and apoptosis was detected by flow cytometry with PI/annexinV staining. Western blotting was used to detected caspase-3 and caspase-8. Neurotoxic and anti-tumor effects were evaluated in animal experiments. Results: DH332 exerts a lower neurotoxicity compared with harmine. It also possesses strong antitumor effects against two B cell lymphoma cell lines with low $IC_{50s}$. Moreover, DH332 could inhibit the proliferation and induce the apoptosis of RAMOS RA.1 and J558 cell lines in a dose-dependent manner. Our results suggest that DH332 triggers apoptosis by mainly activating the caspase signaling pathway. In vivo studies of tumor-bearing BALB/c mice showed that DH332 significantly inhibited growth of J558 xenograft tumors. Conclusions: DH332 exerts effective antitumor activity in vitro and in vivo, and has the potential to be a promising drug candidate for lymphoma therapy.

• 동의생리병리학회지
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• 제27권1호
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• pp.57-62
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• 2013

Alzheimer's disease (AD), one of the most common forms of dementia, is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of ${\beta}$-amyloid ($A{\beta}$) peptides of 40-42 residues, which are generated by processing of amyloid precursor protein (APP). $A{\beta}$ has been believed to be neurotoxic and now is also considered to have a role on the mechanism of memory dysfunction. Here, we show that MeOH extract from stem bark of Platycarya strobilacea Sieb. et. Zucc. (PSM) affects on the processing of APP from the APPswe over-expressing Neuro2a cell line. We found that PSM may regulate the processing of APP and increase the sAPP${\alpha}$. PSM does not change the protein level of presenilin and nicastrin, however, it reduces the protein expression level of BACE1. In addition, PSM reduces the secretion level of $A{\beta}42$ and $A{\beta}40$ from the cell line without toxicity. We suggest that Platycarya strobilacea may be useful as a herbal medicine to treat Alzheimer's disease.

• 생물정신의학
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• 제15권3호
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• pp.175-185
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• 2008

Accumulating evidence has suggested the existence of reciprocal communication between immune, endocrine, and neurotransmitter system. Cytokine hypothesis of depression implies that increased pro-inflammatory cytokine such as -1, IL-6, IL-12, TNF-${\alpha}$, and IFN-${\gamma}$ in major depression, acting neuromodulators, play a key role in the mediation of behavioral, neuroendocrine, and neurochemical disturbances in depression. Concerning the relation between cytokines and serotonin metabolism, pro-inflammatory cytokines have profound effects on the metabolism of brain serotonin through the enzyme indoleamine-2,3-dioxygenase(IDO) that metabolizes tryptophan, the precursor of 5-HT to neurodegenerative quinolinate and neuroprotective kynurenate. The neurodegeneration process is reinforced by the neurotoxic effect of the hypercortisolemia during depression. From this perspective, it is possible that efficacy of antidepressants in the treatment of depression may, at least in part, rely on downregulation of pro-inflammatory cytokine synthesis. So, the use of cytokine synthesis inhibitors or cytokine antagonists may be a new treatment approach in depression. However, at present the question whether cytokines play a causal role in the onset of depression or are mere epiphenomena sustaining depressive symptoms remains to be elucidated. Nevertheless, cytokine hypothesis has created new perspectives in the study of psychological and pathophysiological mechanism that are associated with major depression, as well as the prospect for developing a new generation antidepressants.

• The Journal of Korean Physical Therapy
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• 제13권1호
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• pp.219-227
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• 2001

Capsaicin. a vanillyl amide(8-methy1-N-vanilly1-6-nonenamide) with a molecular weight of 305.42, was substance, interrupting the pain conducting pathway Until recently the neurotoxic effects of Capsaicin to adult animals were thought to be limited to the peripheral nervous system. But several reports suggest the possibility of central nervous system changes after Capsaicin administration to the adult rat. Capsaicin desensitization is defined as long lasting, reversible suppression of sensory neuron activity. How fast and for how long the desensitization develops is related to the dose and time of exposure to Capsaicin, and the interval between consecutive dosing. In the long term Capsaicin treatment can lead to morphological degeneration and changes in some small sensory neurons, predominantly unmyelinated C fiber afferent nerve fibers. Clinical interest has recently been roused by evidence that Capsaicin's desensitizing action may be of therapeutic value and that an endogenous Capsaicin-1 ike substance may exist. This study summarizes the fundamental knowledge(mechanism, receptors, et al of Capsaicin) of Capsaicin for physical therapists.

• 동의생리병리학회지
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• 제30권1호
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• pp.33-39
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• 2016

Alzheimer's disease(AD), one of the most common forms of dementia, is characterized pathologically by the presence of intracellular neurofibrillary tangles and deposition of β-amyloid(Aβ) peptides of 40-42 residues. Aβ has been believed to be neurotoxic and now is also considered to have a role on the mechanism of memory dysfunction. Only a few acetylcholinesterase(AChE) inhibitors have been developed for treatment of AD, although the numbers of patients are rapidly increasing within aging society. Here, we show that ethanol extract of Rosae Rugosae Flos(RR) or its butanol fraction reduce the enzyme activity of AChE and BACE1(β-site APP cleaving enzyme 1). Furthermore, We found that RR inhibits Aβ aggregation and removes Aβ aggregates by Transmission electron microscopy(TEM). In addition, RR reduces the free radical of 2, 2-diphenyl-1-picrylhydrazyl(DPPH). We suggest that Rosae Rugosae Flos may be useful as a herbal medicine to treat AD.

• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2003년도 추계국제학술대회
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• pp.177-177
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• 2003

Methylmercury (MeHg) is a well-known neurotoxicant that causes severe damage to the central nervous system in humans. Many reports have shown that MeHg is poisonous to human body through contaminated foods and has released into the environment. Despite many studies on the pathogenesis of MeHg-induced central neuropathy, no useful mechanism of toxicity has been established so far. In this study, suppressive subtractive hybridization (SSH) was performed to identify differentially expressed genes on human neuroblastoma cell line, SH-SY5Y treated with DMSO and MeHg (6.25 uM) for 6 hr. Differentially expressed cDNA clones were sequenced and were screened by dot blot to eliminate false positive clones. 13 of 35 screened genes were confirmed using real time RT-PCR. These genes include EB1,90-kDa heat-shock protein, chromosome condensation-related SMC-associated protein and brain peptide Al, etc. Analysis of these genes may provide an insight into the neurotoxic effects of MeHg in human neuronal cells and a possibility to develop more efficient and exact monitoring system of heavy metals as ubiquitous environmental pollutants.