• Journal of Ginseng Research
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• 제24권1호
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• pp.8-17
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• 2000

스테로이드 호르몬의 일종인 에스트로젠은 생식기능에 영향을 미치는 것 외에 학습 및 기억과 관련된 기능에도 영향을 미치는 것으로 알려져 있다. 최근, 에스트로젠은 기억과 관련된 뇌세포 신 경망의 발달과 뇌 기능 장애를 방지할 수 있다는 부분에서 상당한 관심의 대상이되고 있다. 그러나 에스트로젠 대체 치료가 폐경기의 많은 여성들에게 도움을 주기도 하지만 여러 부작용을 유발하는 것으로도 알려져 있다 인삼 역시도 스테로이드 특성을 보이며 에스트로젠과 유사한 화학구조를 가지는 여러 성분을 가지고 있다. 본 실험의 목적은 첫째로 공간 기억력을 측정하기에 여러 장점을 가지고 있으면서 다른 어떠한 행동학적 실험보다 학습과 기억의 동물 모텔로 잘 알려진 방법인 Morris water maze를 이용하여 에스트로젠의 효과를 확인하고, 두 번째는 인삼이 학습과 기억에서 에스트로젠과 같은 효과를 나타낼 수 있는지를 확인하는 것이다. 본 실험은 인위적으로 난소를 제거한 쥐에 17$\beta$-estradiol(100~250 $\mu\textrm{g}$/ml), panaxadiol(PD), panaxatriol(PT) sapo-nins(15~100 $\mu\textrm{g}$/ml)을 sesame oil에 녹인 capsule을 implant했다. 첫 번째 실험에서 난소를 제거한 쥐에 에스트로젠을 투입했을때 학습과 기억의 효과를 확인했다. 두 번째 실험에서는 난소를 제거한 쥐에 3가지 다른 농도에서의 PD, PT를 투입했을 때 학습과 기억에 대한 에스트로젠의 효과와 비교해 보았다. 2주 동안의implant 후 water maze 실험결과 세 그룹 모두 난소를 제거한 그룹보다 기억력이 향상되었다 이러한 결과를 토대로 에스트로젠이 학습과 기억에 영향을 준다는 것을 확인할 수 있었고 PD, PT 또한 학습과 기억에 관련된 행동에서 에스트로젠과 같은 효과를 나타낼 수 있다는 것을 확인할 수 있었다. 이러한 동물모델에서의 연구를 통하여 인삼이 에스트로젠 장기결핍치료에서 나타나는 여러 호르몬 부작용을 극복할 수 있는 에스트로젠 대체물질로 개발되어 기억력 저하를 수반하는 Alzheimer's disease 및 여러 퇴행성 중추신경 질환의 치료제로 대체의학의 natural compound이용에 그 기초 기전을 제공할 수 있으리라 여긴다.

• Korean Journal of Acupuncture
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• 제39권4호
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• pp.142-151
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• 2022

Objectives : Parkinson's disease (PD) is a neurodegenerative disorder threatening the quality of life and highly occurred in over 65 years old. Gastrodia elata Blume (GEB), a traditional medicine used for the treatment of headache and convulsion, has been reported to have neuroprotective effect. This study was designed to investigate the neuroprotective effect of GEB and the proteomic changes in the substantia nigra (SN) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Methods : Male eleven-week-old C57BL/6 mice were intraperitoneally injected with 30 mg/kg of MPTP at 24-h intervals for 5 days. Two hours after the daily MPTP injection, the mice were orally administered 800 mg/kg of GEB extract, which continued for 7 days beyond the MPTP injections, for a total of 12 consecutive days. Two hours after the final GEB administration, the brain samples were collected, and dopaminergic neuronal death and proteomic changes in the SN were evaluated. Results : GEB prevented the MPTP-induced dopaminergic neuronal death and regulated the expression of 11 proteins including thimet oligopeptidase, T-complex protein 1, glycine tRNA ligase, and pyruvate kinase isozymes M1. Conclusions : GEB prevents MPTP-induced dopaminergic neuronal death by regulating the proteins in the SN.

• Childhood Kidney Diseases
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• 제14권2호
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• pp.166-173
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• 2010

목 적 : 복막투석환자에서 복막의 용질이동성에 영향을 미치는 요인으로 유전적 요인과 임상적 요인이 있다. 복막평형검사는 복막투석환자의 복막 용질이동속도를 평가하는 데에 유용한 검사로, 본 연구에서는 소아 복막투석 환자에서 복막평형검사 결과를 이용하여 혈관내피성장인자(VEGF)의 유전자 다형성과 복막 용질이동성의 상관관계를 연구하였다. 방 법 : 서울대학교 어린이병원과 삼성서울병원의 소아 복막투석환자 중에서 복막염의 병력이 없고 복막투석 시작한 지 1년 이내에 복막평형검사가 시행된 환자를 대상으로 하였다. VEGF 유전자 -2578 C/A, -14978T/C, -1154G/A, -634G/C, +936 C/T의 단일 유전자다형성분석을 시행하였고 VEGF 유전자 다형성의 분포와 복막평형검사 결과간의 상관관계를 분석하였다. 결 과 : 복막평형검사를 분석한 결과, 4시간 크레아티닌의 투석액/혈장비(D/P creatinine)는 $0.56{\pm}0.13$였고 4시간 투석액/0시간투석액포도당비(D/$D_0$ glucose)는 $0.43{\pm}0.11$였다. 배수체 CTGGC의 이형접합체 또는 동형접합체인 경우가 배수체 CTGGC를 가지지 않은 경우에 비해 높은 4시간 D/P creatinine ($0.67{\pm}0.12$ vs $0.50{\pm}0.09$, P=0.007)과 은 4시간 D/$D_0$ glucose ($0.35{\pm}0.12$ vs $0.47{\pm}0.08$, P=0.037)를 보였다. 결 론 : VEGF 유전자 다형성은 복막 용질이동성에 영향을 미칠 수 있다.

• The Korean Journal of Physiology and Pharmacology
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• 제20권4호
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• pp.399-406
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• 2016

Early life neuronal exposure to environmental toxicants has been suggested to be an important etiology of neurodegenerative disease development. Perfluorohexanesulfonate (PFHxS), one of the major perfluoroalkyl compounds, is widely distributed environmental contaminants. We have reported that PFHxS induces neuronal apoptosis via ERK-mediated pathway. Imperatorin is a furanocoumarin found in various edible plants and has a wide range of pharmacological effects including neuroprotection. In this study, the effects of imperatorin on PFHxS-induced neuronal apoptosis and the underlying mechanisms are examined using cerebellar granule cells (CGC). CGC were isolated from seven-day old rats and were grown in culture for seven days. Caspase-3 activity and TUNEL staining were used to determine neuronal apoptosis. PFHxS-induced apoptosis of CGC was significantly reduced by imperatorin and PD98059, an ERK pathway inhibitor. PFHxS induced a persistent increase in intracellular calcium, which was significantly blocked by imperatorin, NMDA receptor antagonist, MK801 and the L-type voltage-dependent calcium channel blockers, diltiazem and nifedipine. The activation of caspase-3 by PFHxS was also inhibited by MK801, diltiazem and nifedipine. PFHxS-increased ERK activation was inhibited by imperatorin, MK801, diltiazem and nifedipine. Taken together, imperatorin protects CGC against PFHxS-induced apoptosis via inhibition of NMDA receptor/intracellular calcium-mediated ERK pathway.

• 전기학회논문지
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• 제62권7호
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• pp.1009-1013
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• 2013

In this study, we developed a fiber-optic goniometer for the continuous measurement of knee joint angle which provides important medical information on Alzheimer's disease. The fiber-optic goniometer is composed of a light-emitting diode (LED), a plastic optical fiber (POF), and a voltage output photodiode (PD). As a sensing part of the fiber-optic goniometer, a unclad fiber with regular intervals of 1 mm was fabricated to improve efficiency of bending loss according to the angle variation of knee joint. The emitting light with a center wavelength of 470 nm from a LED is guided by a POF to the PD, the transmitted light is then attenuated by the bending loss inside the bent POF. The intensity variation of the light transmitted from the POF gives rise to a change in output voltage in the fiber-optic goniometer. Therefore, we measured the real-time output voltage of the proposed fiber-optic goniometer using the unclad fiber according to the knee joint angle. Through the repeated experiments, the fiber-optic goniometer shows that it has a reversibility and a wide measurable angle range.

• Journal of Periodontal and Implant Science
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• 제36권3호
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• pp.653-659
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• 2006

Oral malodor may cause a significant social or psychological handicap to those suffering from it. Oral malodor has been correlated with the concentration of volatile sulfur compounds (VSC) produced in the oral cavity. Specific bacteria identified in the production of VSC have been reported and many of these bacteria are commonly suspected periodontal pathogens. The aim of this study was to estimate the change of the VSC concentration after periodontal treatment, Twenty subjects with probing depth $(PD)\;{\geq}5mm$ (experimental group) and 20 subjects with PD<5mm (control group) participated. VSC concentration measurement was made with gas chromatography. VSC concentration was measured at pre-treatment, 2 weeks after scaling and 1 month after periodontal treatment(root planning and flap operation). Maximum probing depth and bleeding on probing(BOP) were also examed at pretreatment and 1 month after periodontal treatment, The conclusions were as follow: 1. In the experimental group VSC concentration and CH3SH/H2S ratio were higher than control group. (p<0.05) 2. Both VSC concentration and CH3SH/H2S ratio showed decrease after periodontal treatment, But only CH3SH/H2S ratio after 1 month periodontal treatment was statistically significantly different from pre-treatment. (p<0.05) 3. CH3SH/H2S ratio tended to be on increase according to maximum probing depth and bleeding on probing. Periodontal disease could be a factor that caused oral malodor and oral malodor could be decreased after periodontal treatment.

• Bulletin of the Korean Chemical Society
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• 제28권12호
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• pp.2329-2332
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• 2007

Salsolinol, endogenous neurotoxin, is known to be involved in the pathogenesis of Parkinson's disease (PD). In the present study, we have investigated the oxidative damage of DNA induced by the reaction of salsolinol with Cu,Zn-SOD. When plasmid DNA incubated with salsolinol and Cu,Zn-SOD, DNA cleavage was proportional to the concentrations of salsolinol and Cu,Zn-SOD. The salsolinol/Cu,Zn-SOD system-mediated DNA cleavage was significantly inhibited by radical scavengers such as mannitol, ethanol and thiourea. These results indicated that free radicals might participate in DNA cleavage by the salsolinol/Cu,Zn-SOD system. Spectrophotometric study using a thiobarbituric acid showed that hydroxyl radical formation was proportional to the concentration of salsolinol and was inhibited by radical scavengers. These results indicated that hydroxyl radical generated in the reaction of salsolinol with Cu,Zn-SOD was implicated in the DNA cleavage. Catalase and copper chelators inhibited DNA cleavage and the production of hydroxyl radicals. These results suggest that DNA cleavage is mediated in the reaction of salsolinol with Cu,Zn-SOD via the generation of hydroxyl radical by a combination of the oxidation reaction of salsolinol and Fenton-like reaction of free copper ions released from oxidatively damaged SOD.

• Annals of Clinical Neurophysiology
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• 제8권2호
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• pp.107-124
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• 2006

The basal ganglia are a group of nuclei located in the deep portion of the brain. Along with the cerebellum, the basal ganglia have a major role in controlling human voluntary movements, and their dysfunction is apparently responsible for various involuntary movements. Although the exact mechanism of how the basal ganglia control movements has yet to be clarified, the model of focused selection (through the direct pathway) and tonic inhibition (via the indirect pathway) is proposed to be a principal functional model of the basal ganglia. Parkinson's disease (PD) is classically characterized by bradykinesia, rigidity and tremor-at-rest. All features seem to be associated with dopamine depletion resulting from the degeneration of the nigrostriatal pathway, which produces reduced activity of the direct pathway and a concurrent enhancement of excitatory output from STN. This change may result in increased tonic background inhibition and reduced focused selection via the direct pathway, causing difficulties in performing voluntary movements selectively. However, it has not been possible to define a single underlying pathophysiologic mechanism that explains all parkinsonian symptoms. Here the data that give separate understanding to each of the three classic features are discussed.

• 대한의생명과학회지
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• 제17권2호
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• pp.167-171
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• 2011

[ ${\alpha}$ ]synuclein (${\alpha}$-syn) is implicated in the pathogenesis of Parkinson's disease (PD) and other related diseases. We have previously reported that ${\alpha}$-syn binds to the cell membranes in a transient and reversible manner. However, little is known about the physiologic function and/or consequence of this association. Here, we examined whether chemically induced perturbations to the cellular membranes enhance the binding of ${\alpha}$-syn, based on hypothesis that ${\alpha}$-syn may play a role in maintenance of membrane integrity or repair. We induced membrane perturbations or alterations in ${\alpha}$-syn-overexpressing human neuroblastoma cells (SH-SY5Y) by treating the cells with hydrogen peroxide ($H_2O_2$) or oleic acid. In addition, membranes fractionated from these cells were perturbed by treating them with proteinase K or chloroform. Dynamic interaction of ${\alpha}$-syn to the membranes was analyzed by the chemical cross-linking assay that we developed in the previous study. We found that membrane interaction of ${\alpha}$-syn was increased upon treatment with membrane-perturbing reagents in a dose and time dependent manner. These results suggest that perturbations in the cellular membranes cause increased binding of ${\alpha}$-syn, and this may have significant implication in the physiological function of ${\alpha}$-syn in cells.

• Korean Journal of Radiology
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• 제24권3호
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• pp.247-258
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• 2023

Objective: To localize the neuroanatomical substrate of rapid eye movement sleep behavior disorder (RBD) and to investigate the neuroanatomical locational relationship between RBD and α-synucleinopathy neurodegenerative diseases. Materials and Methods: Using a systematic PubMed search, we identified 19 patients with lesions in different brain regions that caused RBD. First, lesion network mapping was applied to confirm whether the lesion locations causing RBD corresponded to a common brain network. Second, the literature-based RBD lesion network map was validated using neuroimaging findings and locations of brain pathologies at post-mortem in patients with idiopathic RBD (iRBD) who were identified by independent systematic literature search using PubMed. Finally, we assessed the locational relationship between the sites of pathological alterations at the preclinical stage in α-synucleinopathy neurodegenerative diseases and the brain network for RBD. Results: The lesion network mapping showed lesions causing RBD to be localized to a common brain network defined by connectivity to the pons (including the locus coeruleus, dorsal raphe nucleus, central superior nucleus, and ventrolateral periaqueductal gray), regardless of the lesion location. The positive regions in the pons were replicated by the neuroimaging findings in an independent group of patients with iRBD and it coincided with the reported pathological alterations at post-mortem in patients with iRBD. Furthermore, all brain pathological sites at preclinical stages (Braak stages 1-2) in Parkinson's disease (PD) and at brainstem Lewy body disease in dementia with Lewy bodies (DLB) were involved in the brain network identified for RBD. Conclusion: The brain network defined by connectivity to positive pons regions might be the regulatory network loop inducing RBD in humans. In addition, our results suggested that the underlying cause of high phenoconversion rate from iRBD to neurodegenerative α-synucleinopathy might be pathological changes in the preclinical stage of α-synucleinopathy located at the regulatory network loop of RBD.