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学科主题: 公共卫生
题名:
Epigallocatechin-3-gallate protects pro-inflammatory cytokine induced injuries in insulin-producing cells through the mitochondrial pathway
作者: Zhang, Zhaofeng; Ding, Ye; Dai, Xiaoqian; Wang, Junbo; Li, Yong
关键词: Epigallocatechin-3-gallate ; Pro-inflammatory cytokine ; Insulin-producing cell ; Mitochondrial pathway
刊名: EUROPEAN JOURNAL OF PHARMACOLOGY
发表日期: 2011-11-16
DOI: 10.1016/j.ejphar.2011.08.033
卷: 670, 期:1, 页:311-316
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy
研究领域[WOS]: Pharmacology & Pharmacy
关键词[WOS]: PANCREATIC BETA-CELLS ; INDUCED APOPTOSIS ; HIGH GLUCOSE ; GREEN TEA ; CARDIOVASCULAR-DISEASE ; METABOLIC SIGNALS ; DOWN-REGULATION ; INHIBITION ; EXPRESSION ; EXPOSURE
英文摘要:

Pro-inflammatory cytokine-mediated pancreatic beta-cell dysfunction is a key pathological event in type 1 diabetes mellitus. There are few studies about the protection of epigallocatechin-3-gallate (EGCG) against pro-inflammatory cytokine-induced beta-cell apoptosis. To examine the direct effects of EGCG on beta-cells, insulin-producing RINm5F cells were exposed to a combination of recombinant interleukin-1beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma), with or without EGCG pretreatment for 24 h. Cell death was monitored by the MTT assay. Glucose-stimulated insulin release was measured using radio immunoassay. Intracellular reactive oxygen species was examined with dichlorofluorescein (DCF) fluorescence by flow cytometry. To evaluate RINm5F cells mitochondrial function, change in mitochondrial membrane potential, intracellular ATP levels, and nitric oxide was assessed. The expression of cytochrome c, Bax. Bcl-2, and iNOS proteins was measured by western blotting. In the present study, EGCG pretreatment protected against cytokines inducing cell death and restored glucose stimulated-insulin secretion in RINm5F cells. EGCG reduced the cytokine-induced generation of reactive oxygen species, the loss of mitochondrial membrane potential (Delta psi m), the release of cytochrome c from the mitochondria, and translocation of Bax protein to the mitochondria from the cytosol. EGCG pretreatment prevented cytokine-induced iNOS overexpression and NO generation. In summary, pro-inflammatory cytokines lead to a reduction of glucose-induced insulin secretion, mitochondrial activity and viability in RINm5F cells. The pro-inflammatory cytokine-induced effects can be prevented by EGCG pretreatment via the mitochondrial pathway. (C) 2011 Elsevier B.V. All rights reserved.

语种: 英语
所属项目编号: 2006BAD27B01
项目资助者: Ministry of Science and Technology of the People&prime ; s Republic of China
WOS记录号: WOS:000296550500043
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54865
Appears in Collections:北京大学公共卫生学院_期刊论文

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作者单位: Peking Univ, Dept Food Hyg & Nutr, Sch Publ Hlth, Beijing 100191, Peoples R China

Recommended Citation:
Zhang, Zhaofeng,Ding, Ye,Dai, Xiaoqian,et al. Epigallocatechin-3-gallate protects pro-inflammatory cytokine induced injuries in insulin-producing cells through the mitochondrial pathway[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2011,670(1):311-316.
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