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High glucose stimulates TNF alpha and MCP-1 expression in rat microglia via ROS and NF-kappa B pathways
Quan, Yi1; Jiang, Chang-tao1; Xue, Bing3,4; Zhu, Shi-gong1; Wang, Xian1,2
关键词high glucose microglia tumor necrosis factor alpha monocyte chemotactic protein-1 reactive oxygen species NF-kappa B
刊名ACTA PHARMACOLOGICA SINICA
2011-02-01
DOI10.1038/aps.2010.174
32期:2页:188-193
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Chemistry, Multidisciplinary ; Pharmacology & Pharmacy
研究领域[WOS]Chemistry ; Pharmacology & Pharmacy
关键词[WOS]TUMOR-NECROSIS-FACTOR ; MONOCYTE CHEMOATTRACTANT PROTEIN-1 ; NERVOUS-SYSTEM COMPLICATIONS ; INDUCED APOPTOSIS ; C-PEPTIDE ; OXIDATIVE STRESS ; DIABETIC KIDNEY ; HYPERGLYCEMIA ; CELLS ; ACTIVATION
英文摘要

Aim: To investigate whether high glucose stimulates the expression of inflammatory cytokines and the possible mechanisms involved.

Methods: ELISA and real-time PCR were used to determine the expression of the inflammatory factors, and a chemiluminescence assay was used to measure the production of reactive oxygen species (ROS).

Results: Compared to low glucose (10 mmol/L), treatment with high glucose (35 mmol/L) increased the secretion of tumor necrosis factor (TNF)alpha and monocyte chemotactic protein-1 (MCP-1), but not interleukin (IL)-1 beta and IL-6, in a time-dependent manner in primary cultured rat microglia. The mRNA expression of TNF alpha and MCP-1 also increased in response to high glucose. This upregulation was specific to high glucose because it was not observed in the osmotic control. High-glucose treatment stimulated the formation of ROS. Furthermore, treatment with the ROS scavenger NAC significantly reduced the high glucose-induced TNF alpha and MCP-1 secretion. In addition, the nuclear factor kappa B (NF-kappa B) inhibitors MG132 and PDTC completely blocked the high glucose-induced TNF alpha and MCP-1 secretion.

Conclusion: We found that high glucose induces TNFa and MCP-1 secretion as well as mRNA expression in rat microglia in vitro, and this effect is mediated by the ROS and NF-kappa B pathways.

语种英语
WOS记录号WOS:000286968200008
项目编号2006CB503802 ; 30330250
资助机构Major National Basic Research Program of China ; Program for Changjiang Scholars and Innovative Research Team in Universities ; National Natural Science Foundation of China
引用统计
被引频次:43[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65482
专题北京大学基础医学院
作者单位1.Peking Univ, Neurosci Res Inst, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
3.Peking Univ, Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
4.Peking Univ, Minist Educ, Key Lab Neurosci, Dept Neurobiol, Beijing 100191, Peoples R China
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GB/T 7714
Quan, Yi,Jiang, Chang-tao,Xue, Bing,et al. High glucose stimulates TNF alpha and MCP-1 expression in rat microglia via ROS and NF-kappa B pathways[J]. ACTA PHARMACOLOGICA SINICA,2011,32(2):188-193.
APA Quan, Yi,Jiang, Chang-tao,Xue, Bing,Zhu, Shi-gong,&Wang, Xian.(2011).High glucose stimulates TNF alpha and MCP-1 expression in rat microglia via ROS and NF-kappa B pathways.ACTA PHARMACOLOGICA SINICA,32(2),188-193.
MLA Quan, Yi,et al."High glucose stimulates TNF alpha and MCP-1 expression in rat microglia via ROS and NF-kappa B pathways".ACTA PHARMACOLOGICA SINICA 32.2(2011):188-193.
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