• Journal of Applied Biological Chemistry
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• v.64 no.3
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• pp.299-307
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• 2021

Accumulation of amyloid beta (Aβ) and oxidative stress are the most common reason of Alzheimer's disease (AD). In the present study, we investigated the cognitive improvement effects of butanol (BuOH) fraction from Momordica charantia in Aβ_25-35-induced AD mouse model. To develop an AD mouse model, mice were received injection of Aβ_25-35, and then orally administered BuOH fraction from M. charantia at doses of 100 and 200 mg/kg/day during 14 days. In the T-maze and novel object recognition test, administration of BuOH fraction from M. charantia L. at doses of 100 and 200 mg/kg/day improved spatial ability and novel object recognition by increased explorations of novel route and new object. In addition, BuOH fraction of M. charantia-administered groups improved learning and memory abilities by decreased time to reach hidden platform in Morris water maze test. Oral administration of BuOH fraction from M. charantia significantly inhibited lipid peroxidation and nitric oxide levels in the brain, liver, and kidney compared with Aβ_25-35-induced control group. These results indicated that BuOH fraction of M. charantia improved Aβ_25-35-induced cognitive impairment by attenuating oxidative stress. Therefore, M. charantia could be useful for protection from Aβ_25-35-induced cognitive impairment.

• Proceedings of the KSAR Conference
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• 2002.06a
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• pp.199.2-200
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• 2002

• 한국약용작물학회:학술대회논문집
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• 2006.04a
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• pp.121-135
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• 2006

• Bulletin of the Korean Chemical Society
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• v.33 no.12
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• pp.4281-4281
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• 2012

• 한국전자현미경학회:학술대회논문집
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• 1998.05a
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• pp.65-65
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• 1998

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.207.1-207.1
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• 2000

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.101.1-101.1
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• 2002

• The Korean Journal of Cytopathology
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• v.11 no.2
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• pp.99-102
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• 2000

Pulmonary amyloid deposition generally occurs with concurrent primary systemic amyloidosis. Localized forms of pulmonary amyloidosis are rare and appear most frequently as an incidental finding on chest radiographs. We present a case of nodular pulmonary amyloid tumor suggested by fine needle aspiration cytology(FNAC) and confirmed by histology examination with the polarizing light microscopy. A 41-year-old woman presented with ill-defined nodules. In the middle and lower lobes of both lungs. FNAC of the nodules revealed waxy, acellular amorphous fragments. Thoracotomy for diagnosis may be avoided by FNAC diagnosis of this unusual lesion.

• BMB Reports
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• v.36 no.5
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• pp.488-492
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• 2003

Neurofilament-L (NF-L) is a major element of neuronal cytoskeletons and known to be important for neuronal survival in vivo. Since oxidative stress might play a critical role in the pathogenesis of neurodegenerative diseases, we investigated the role of copper and peroxide in the modification of NF-L. When disassembled NF-L was incubated with copper ion and hydrogen peroxide, then the aggregation of protein was proportional to copper and hydrogen peroxide concentrations. Dityrosine crosslink formation was obtained in copper-mediated NF-L aggregates. The copper-mediated modification of NF-L was significantly inhibited by thiol antioxidants, N-acetylcysteine, glutathione, and thiourea. A thioflavin-T binding assay was performed to determine whether the copper/$H_2O_2$ system-induced in vitro aggregation of NF-L displays amyloid-like characteristics. The aggregate of NF-L displayed thioflavin T reactivity, which was reminiscent of amyloid. This study suggests that copper-mediated NF-L modification might be closely related to oxidative reactions which may play a critical role in neurodegenerative diseases.

• Korean Journal of Biological Psychiatry
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• v.10 no.2
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• pp.97-106
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• 2003

Criticisms about amyloid cascade hypothesis of Alzheimer's disease(AD) are based on the findings, first, that the degree of dementia does not correlate with the number of plaques, and second, that the neurofibrillary tangle formation seems to predate plaque formation. In addition, neurofibrillary tangle counts correlate well with the degree of cognitive impairment. These findings suggest the independent importance of tau abnormality in AD research which is involved in the neurofibrillary tangle formation. Recently, tau pathology without amyloid deposits and mutations in tau protein gene were reported to be the major pathogenic mechanism in Pick's disease, progressive supranuclear palsy, corticobasal degeneration and FTDP-17(frontotemporal dementia and parkinsonism linked with chromosome 17). These data suggest that understanding the causes and consequences of tau dysfunction might give new clinical and therapeutic solutions to many known tauopathies.