• Journal of Oriental Neuropsychiatry
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• v.19 no.3
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• pp.179-193
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• 2008

Objective: The antioxidant and anti-Alzheimer effects of Semen Ziziphi Spinosae (SZS) water extract against the amyloid beta peptide (1-42) or H202-induced oxidative damage and cell death were investigated in rat pheochromocytoma line PC 12. Methods: The cells were incubated with SZS water extract and oxidative damage-inducing materials, amyloid beta peptide (1-42) or H2O2 for 24 h. The cellular viability was assessed by WST-1 assay, cytotoxic damage by LDH activity assay, oxidative damages of cells by fluorescence spectrophotometric method, and apoptosis by TUNEL staining assay. Results and Conclusions: 1. Preincubation of the cells with SZS water extract prior to amyloid beta peptide (1-42) (2 uM) or H2O2 (30 uM) exposure elevated the cell survival close to the control and decreased the level of LDH activity and the fluorescence from the cell homogenates and TUNEL staining of the cells, compared to only amyloid beta peptide (1-42) (2 uM) or H2O2 (30 uM) treated conditions. 2. Our study suggests that Semen Ziziphi Spinosae (SZS) water extract has protective effects against amyloid beta peptide (1-42) or H2O2-induced cell toxicity through the antioxidation mechanism, which might be beneficial for the treatment of Alzheimer's disease.

• Journal of Microbiology and Biotechnology
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• v.27 no.11
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• pp.2044-2051
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• 2017

The main pathological hallmark of Alzheimer's disease is the deposition of amyloid-beta ($A{\beta}$) peptides in the brain. $A{\beta}$ has been widely used to mimic several aspects of Alzheimer's disease. However, several characteristics of amyloid-induced Alzheimer's disease pathology are not well established, especially in mice. The present study aimed to develop a new Alzheimer's disease model by investigating how $A{\beta}$ can be effectively aggregated using prokaryotes and eukaryotes. To express the $A{\beta}42$ complex in HEK293 cells, we cloned the $A{\beta}42$ region in a tandem repeat and incorporated the resulting construct into a eukaryotic expression vector. Following transfection into HEK293 cells via lipofection, cell viability assay and western blotting analysis revealed that exogenous $A{\beta}42$ can induce cell death and apoptosis. In addition, recombinant His-tagged $A{\beta}42$ was successfully expressed in Escherichia coli BL21 (DE3) and not only readily formed $A{\beta}$ complexes, but also inhibited the proliferation of SH-SY5Y cells and E. coli. For in vivo testing, recombinant His-tagged $A{\beta}42$ solution ($3{\mu}g/{\mu}l$ in $1{\times}PBS$ containing $1mM\;Ni^{2+}$) was injected stereotaxically into the left and right lateral ventricles of the brains of C57BL/6J mice (n = 8). Control mice were injected with $1{\times}PBS$ containing $1mM\;Ni^{2+}$ following the same procedure. Ten days after the sample injection, the Morris water maze test confirmed that exogenous $A{\beta}$ caused an increase in memory loss. These findings demonstrated that $Ni^{2+}$ is capable of complexing the 50-kDa amyloid and that intracerebroventricular injection of $A{\beta}42$ can lead to cognitive impairment, thereby providing improved Alzheimer's disease models.

• Korean Journal of Biological Psychiatry
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• v.27 no.2
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• pp.94-100
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• 2020

Objectives Amyloid β positron emission tomography (Aβ PET) is widely used as a diagnostic tool in patients who have symptoms of cognitive impairment, however, this diagnostic examination is too expensive. Thus, predicting the positivity of Aβ PET before patients undergo the examination is essential. We aimed to analyze clinical predictors of patients who underwent Aβ PET retrospectively, and to develop a predicting model of Aβ PET positivity. Methods 468 patients who underwent Aβ PET with cognitive impairment were recruited and their clinical indicators were analyzed retrospectively. We specified the primary outcome as Aβ PET positivity, and included variables such as age, sex, body mass index, diastolic blood pressure, systolic blood pressure, education, dementia family history, Mini Mental Status Examination (MMSE), Clinical Dementia Rating (CDR), Clinical Dementia Rating-Sum of Box (CDR-SB), hypertension (HTN), diabetes mellitus (DM) and presence of apolipoprotein E (ApoE) E4 as potential predictors. We developed three final models of amyloid positivity prediction for total subjects, mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia using a multivariate stepwise logistic regression analysis. Receiver operating characteristic (ROC) curve analysis was performed and the area under curve (AUC) value was calculated for the ROC curve. Results Aβ PET negative patients were 49.6% (n = 232), and Aβ PET positive patients were 50.4% (n = 236). In the final model of all subjects, older age, female sex, presence of ApoE E4 and lower MMSE are associated with Aβ PET positivity. The AUC value was 0.296. In the final model of MCI subjects (n = 244), older age and presence of ApoE E4 are associated with Aβ PET positivity. The AUC value was 0.725. In the final model of AD subjects (n = 173), lower MMSE scores, the presence of ApoE E4 and history of HTN are associated with Aβ PET positivity. The AUC value was 0.681. Conclusions The cerebral amyloid positivity model, which was based on commonly available clinical indicators, can be useful for prediction of amyloid PET positivity in MCI or AD patients.

• 한국약용작물학회:학술대회논문집
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• 2007.05a
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• pp.288-289
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• 2007

• 한국약용작물학회:학술대회논문집
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• 2008.11a
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• pp.298-299
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• 2008

• Journal of Chest Surgery
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• v.32 no.11
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• pp.1060-1063
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• 1999

Amyloidosis is a rare disease which is characterized by the deposition of a histochemically specific substance called amyloid in many tissue bodies, and causes various symptoms according to the organs involved. Amyloid is usually recognized by its staining reaction with Congo red stain. Primary pulmonary amyloidosis is very rare. Nodular pulmonary amyloidosis is an uncommon entity that usually manifests itself as an asymptomatic incidental finding on the chest roentgenogram and is misdiagnosed as lung cancer or pulmonary tuberculosis.

• Bulletin of the Korean Chemical Society
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• v.28 no.7
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• pp.1231-1234
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• 2007

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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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)

• 한국약용작물학회:학술대회논문집
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• 2009.05a
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• pp.287-288
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• 2009

• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.188-188
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• 2005