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学科主题: 临床医学
题名:
Xylocoside G Reduces Amyloid-beta Induced Neurotoxicity by Inhibiting NF-kappa B Signaling Pathway in Neuronal Cells
作者: Yu, Yan2,3,4; Zhou, Liang2,3,4; Sun, Miao2,3,4; Zhou, Ting2,3,4; Zhong, Kaiyin2,3,4; Wang, Hecheng2,3,4; Liu, Yi2,3,4; Liu, Xinying2,3,4; Xiao, RuiZhong; Ge, Jia5; Tu, PengFei5; Fan, Dong Sheng1; Lan, Yuan6; Hui, Chen7; Chui, Dehua2,3,4
关键词: Amyloid-beta ; apoptosis ; MAPK ; NF-kappa B ; neuroinflammation ; Xylocoside G
刊名: JOURNAL OF ALZHEIMERS DISEASE
发表日期: 2012
DOI: 10.3233/JAD-2012-110779
卷: 30, 期:2, 页:263-275
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]: ALZHEIMERS-DISEASE BRAIN ; RAT CORTICAL-NEURONS ; INDUCED APOPTOSIS ; NUCLEAR TRANSLOCATION ; CYCLOOXYGENASE-2 ; PROTEIN ; ACTIVATION ; EXPRESSION ; PEPTIDE ; KINASE
英文摘要:

Amyloid-beta (A beta) peptide, which can invoke a cascade of inflammatory responses, is considered to play a causal role in the development and progress of Alzheimer′s disease (AD). Xylocoside G (XG) is an active compound isolated from a traditional Chinese medicinal plant, Itoa orientalis. We have previously reported that XG has neuroprotective effects, of which the mechanism is yet unknown. In this study, we investigated the possible mechanisms underlying neuroprotection of XG against A beta-induced toxicity in SH-SY5Y cells and primary neurons. Pretreatment with XG significantly attenuated the cell viability reduction induced by A beta exposure in a dose dependent manner which was testified by 3-[ 4,5-Dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase release assay. In addition, pretreatment with XG countered the effect of A beta on Bax and Bcl-2 expression and repressed A beta-induced caspase-3 activation, suggesting that the neuroprotective effect of XG is associated with apoptosis regulation. Neuroinflammation has been implicated in A beta-induced neuronal death. XG significantly attenuated A beta-stimulated release of inflammatory factors such as tumor necrosis factor-alpha, interleukin-1 beta, and prostaglandin E-2. It also downregulated the expression of cyclooxygenase-2 in SH-SY5Y cells. Further molecular mechanism studies demonstrated that XG inhibited A beta-induced NF-kappa B p65 translocation, which was probably the result of inhibition of JNK phosphorylation but not ERK or p38 MAPK pathway by XG. This is the first study to demonstrate that XG protects SH-SY5Y cells against A beta-induced inflammation and apoptosis by down-regulating NF-kappa B signaling pathways.

语种: 英语
所属项目编号: 30570533 ; 30670414 ; 30973145 ; 81171015 ; 20090001110058 ; 2012CB911004
项目资助者: National Natural Science Foundation of China (NSFC) ; Ministry of Education ; National High Technology Research and Development Program of China (973 Program)
WOS记录号: WOS:000304400700005
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59148
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, Hlth Sci Ctr, Hosp 3, Neurosci Res Inst,Dept Neurol, Beijing 100191, Peoples R China
2.Peking Univ, Minist Educ, Neurosci Res Inst, Beijing 100191, Peoples R China
3.Peking Univ, Minist Educ, Dept Neurobiol, Key Lab Neurosci, Beijing 100191, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Minist Publ Hlth, Beijing 100191, Peoples R China
5.Peking Univ, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
6.Peking Univ, Med & Hlth Analyt Ctr, Beijing 100191, Peoples R China
7.Capital Univ Med Sci, China Rehabil Res Ctr, Beijing, Peoples R China

Recommended Citation:
Yu, Yan,Zhou, Liang,Sun, Miao,et al. Xylocoside G Reduces Amyloid-beta Induced Neurotoxicity by Inhibiting NF-kappa B Signaling Pathway in Neuronal Cells[J]. JOURNAL OF ALZHEIMERS DISEASE,2012,30(2):263-275.
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