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学科主题: 临床医学
题名:
Celastrol Enhances Cell Viability and Inhibits Amyloid-beta Production Induced by Lipopolysaccharide In Vitro
作者: Zhao, Yan1,2; Zhao, Hailin2; Lobo, Niyati2; Guo, Xiangyang1; Gentleman, Steve M.3; Ma, Daqing2
关键词: Alzheimer&prime ; s disease ; amyloid-beta ; celastrol ; cell signal ; lipopolysaccharide ; neuroinflammation
刊名: JOURNAL OF ALZHEIMERS DISEASE
发表日期: 2014
DOI: 10.3233/JAD-131799
卷: 41, 期:3, 页:835-844
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Neurosciences
研究领域[WOS]: Neurosciences & Neurology
关键词[WOS]: HEAT-SHOCK PROTEINS ; ALZHEIMERS-DISEASE ; ANTIINFLAMMATORY DRUGS ; GENE POLYMORPHISMS ; PRECURSOR PROTEIN ; APOPTOSIS ; ACCUMULATION ; PEPTIDE ; DEATH ; PHOSPHORYLATION
英文摘要:

Background: Neuroinflammation is a notable hallmark of Alzheimer′s disease pathogenesis and can markedly exacerbate amyloid pathology. Celastrol, a pentacyclic-triterpene, has been found to possess anti-inflammatory properties.

Objective: The purpose of this study was to characterize the effects of celastrol on cell viability and amyloid-(A) peptide production induced by lipopolysaccharide (LPS) administration in H4 human neuroglioma cells stably transfected to overexpress human full length APP (H4-APP). Methods: H4-APP cells were exposed to 1, 10, and 100nM of celastrol in the presence of 0.1 g/ ml or 100g/ ml of LPS for 24 hours. The effects of celastrol were determined using MTT cell viability assay, immunohistochemistry, western blot, and ELISA.

Results: Cell viability tests revealed that a dose-dependent death of H4-APP cells following administration of LPS. Moreover, celastrol significantly reduced (p < 0.05) cell death induced by LPS compared to LPS alone. Furthermore, the administration of celastrol was associated with a significant reduction in LPS-stimulated A production compared to LPS alone. Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NF.B activity, phosphorylated glycogen synthase kinase-3 (GSK-3) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, A accumulation together with a reduction of superoxide and hydrogen peroxide generation. HSP-70 siRNA abolished celastrol mediated cytoprotection.

Conclusion: This study demonstrates that celastrol reduced both LPS-induced cell death and A production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NF.B, COX-2, and GSK-3 expression and oxidative stress.

语种: 英语
项目资助者: Chinese Society of Anesthesiology, Beijing, China ; The Alzheimer&prime ; s Society/BUPA foundation, London, UK
WOS记录号: WOS:000339329100020
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54494
Appears in Collections:北京大学第三临床医学院_期刊论文

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作者单位: 1.Peking Univ, Dept Anaesthesiol, Hosp 3, Beijing 100871, Peoples R China
2.Univ London Imperial Coll Sci Technol & Med, Chelsea & Westminster Hosp, Dept Surg & Canc, Fac Med, London, England
3.Univ London Imperial Coll Sci Technol & Med, Dept Med, Neuropathol Unit, London, England

Recommended Citation:
Zhao, Yan,Zhao, Hailin,Lobo, Niyati,et al. Celastrol Enhances Cell Viability and Inhibits Amyloid-beta Production Induced by Lipopolysaccharide In Vitro[J]. JOURNAL OF ALZHEIMERS DISEASE,2014,41(3):835-844.
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