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内质网应激信号通路在棕榈酸诱导的血管内皮细胞凋亡中的作用

许文虎 金春子 王晓龙 陈晨 崔兰

中国药理学通报2017,Vol.33Issue(12):1668-1672,5.
中国药理学通报2017,Vol.33Issue(12):1668-1672,5.DOI:10.3969/j.issn.1001-1978.2017.12.009

内质网应激信号通路在棕榈酸诱导的血管内皮细胞凋亡中的作用

Role of endoplasmic reticulum stress signaling pathway in high fat-induced cell apoptosis in vascular endothelial cells

许文虎 1金春子 2王晓龙 1陈晨 1崔兰1

作者信息

  • 1. 延边大学附属医院心血管内科,吉林 延吉 133000
  • 2. 延边大学附属医院中心实验室,吉林 延吉 133000
  • 折叠

摘要

Abstract

Aim To explore the role of endoplasmic reticulum stress(ERS)signaling pathway in high fat-induced cell apoptosis in human umbilical vein endo-thelial cells(HUVECs). Methods HUVECs were ex-posed to different concentrations of palmitic acid(0. 1, 0. 2,0. 4,0. 8 mmol·L - 1 )for 24 h and different time points of 0. 4 mmol·L - 1 palmitic acid(0,12, 24,48 h). Cell viability was measured by cell count-ing kit(CCK-8),and the protein expressions of ERS signaling pathway protein such as GRP78,CHOP, PERK,IRE1,ATF6 were determined by Western blot. The level of intracellular apoptosis was detected by immunofluorescence. Results HUVECs exposed to palmitic acid at 0. 4 mmol·L - 1 for 24 h showed a de-crease in their viability and an increase in the expres-sion of ERS signaling pathway proteins (GRP78, CHOP,PERK,IRE1,ATF6)(P < 0. 05);cell ap-optotic levels significantly increased(P < 0. 05). The intracellular apoptosis levels in the vascular endothelial cells of ERS signaling pathway inhibitor 4-phenylbutyr-ic acid (4-PBA,10 mmol · L - 1 )were significantly lower than those of the PA group(P < 0. 05). Conclu-sion Activated ERS signaling pathway might play an important role in the treatment of high fat-induced cell apoptosis in vascular endothelial cells.

关键词

内质网应激/棕榈酸/血管内皮细胞/4-苯基丁酸/人脐静脉血管内皮细胞/凋亡

Key words

endoplasmic reticulum stress/palmitic acid/vascular endothelial cell/4-phenylbutyric acid/human umbilical vein endothelial cells/cell apoptosis

分类

医药卫生

引用本文复制引用

许文虎,金春子,王晓龙,陈晨,崔兰..内质网应激信号通路在棕榈酸诱导的血管内皮细胞凋亡中的作用[J].中国药理学通报,2017,33(12):1668-1672,5.

基金项目

国家自然科学基金资助项目(No 81460039) (No 81460039)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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