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Quercetin protects RAW264.7 macrophages from glucosamine-induced apoptosis and lipid accumulation via the endoplasmic reticulum stress pathway
Cai, Xiaxia1; Bao, Lei2; Dai, Xiaoqian1; Ding, Ye1; Zhang, Zhaofeng1; Li, Yong1
关键词quercetin macrophages glucosamine endoplasmic reticulum stress atherosclerosis
刊名MOLECULAR MEDICINE REPORTS
2015-11-01
DOI10.3892/mmr.2015.4340
12期:5页:7545-7553
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Medicine, Research & Experimental
资助者National Natural Science Foundation of China ; National Natural Science Foundation of China
研究领域[WOS]Oncology ; Research & Experimental Medicine
关键词[WOS]HYPERGLYCEMIC MOUSE MODEL ; BLOOD-PRESSURE ; ER STRESS ; ATHEROSCLEROTIC PLAQUES ; CARDIOVASCULAR-DISEASE ; HEPATIC STEATOSIS ; ENDOTHELIAL-CELLS ; GENE-EXPRESSION ; RISK-FACTORS ; BETA-CELLS
英文摘要

It is increasingly recognized that macrophages are a key cell in the development of atherosclerosis. Glucosamine, the product of the hexosamine biosynthetic pathway in diabetes mellitus, can disturb lipid metabolism, induce apoptosis and accelerate atherosclerosis via endoplasmic reticulum (ER) stress in various types of cells. Previous studies have indicated that quercetin possesses antidiabetic, anti-oxidative, anti-inflammatory and anti-apoptotic activities as a flavonoid. Studies have also demonstrated its novel pharmacological properties for inhibiting ER stress. The present study focussed on the effects of quercetin on cell injury and ER stress in glucosamine-induced macrophages. RAW264.7 macrophages were cultured with 15 mM glucosamine, following which the levels of apoptosis, intracellular total and free cholesterol, and apoptosis- and ER stress-associated proteins were measured in the macrophages treated with or without quercetin. Additionally, the ratio of cholestryl ester/total cholesterol was calculated to observe the formation of foam cells. The results demonstrated that apoptosis and abnormal lipid accumulation in the RAW264.7 cells, which was induced by glucosamine, were significantly reversed by quercetin. In addition, quercetin treatment suppressed the increase of C/EBP homologous protein, and inhibited the activation of JNK and caspase-12, which was induced by glucosamine. Quercetin also increased the expression level of full length activating transcriptional factor 6 and decreased the expression of glucose regulated protein 78. Of note, the beneficial effects of quercetin on the glucosamine-induced RAW264.7 cells were reversed by treatment with tunicamycin. These findings suggest that quercetin may have properties to prevent glucosamine-induced apoptosis and lipid accumulation via the ER stress pathway in RAW264.7 macrophages.

语种英语
所属项目编号81172652
资助者National Natural Science Foundation of China ; National Natural Science Foundation of China
WOS记录号WOS:000364889100046
引用统计
被引频次:6[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/400002259/62641
专题北京大学公共卫生学院
作者单位1.Peking Univ, Dept Food Hyg & Nutr, Sch Publ Hlth, Beijing 100191, Peoples R China
2.Peking Univ, Int Hosp, Dept Clin Nutr, Beijing 102206, Peoples R China
推荐引用方式
GB/T 7714
Cai, Xiaxia,Bao, Lei,Dai, Xiaoqian,et al. Quercetin protects RAW264.7 macrophages from glucosamine-induced apoptosis and lipid accumulation via the endoplasmic reticulum stress pathway[J]. MOLECULAR MEDICINE REPORTS,2015,12(5):7545-7553.
APA Cai, Xiaxia,Bao, Lei,Dai, Xiaoqian,Ding, Ye,Zhang, Zhaofeng,&Li, Yong.(2015).Quercetin protects RAW264.7 macrophages from glucosamine-induced apoptosis and lipid accumulation via the endoplasmic reticulum stress pathway.MOLECULAR MEDICINE REPORTS,12(5),7545-7553.
MLA Cai, Xiaxia,et al."Quercetin protects RAW264.7 macrophages from glucosamine-induced apoptosis and lipid accumulation via the endoplasmic reticulum stress pathway".MOLECULAR MEDICINE REPORTS 12.5(2015):7545-7553.
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