[1]严静,陈俊,艾志兵,等.sEHi对颈动脉狭窄患者内皮祖细胞增殖及PI3K/Akt信号通路的影响[J].卒中与神经疾病杂志,2017,24(05):402-406.[doi:10.3969/j.issn.1007-0478.2017.05.005]
　Yan Jing,Chen Jun,Ai Zhibing,et al.The effect of soluble epoxide hydrolase inhibitor on proliferation and PI3K/Akt signaling pathway in endothelial progenitor cell s from patients with carotid stenosis[J].Stroke and Nervous Diseases,2017,24(05):402-406.[doi:10.3969/j.issn.1007-0478.2017.05.005]
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sEHi对颈动脉狭窄患者内皮祖细胞增殖及PI3K/Akt信号通路的影响()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
第24卷
期数:
2017年05期
页码:
402-406
栏目:
论 著
出版日期:
2017-10-26

文章信息/Info

Title:
The effect of soluble epoxide hydrolase inhibitor on proliferation and PI3K/Akt signaling pathway in endothelial progenitor cell s from patients with carotid stenosis
文章编号:
1007-0478(2017)05-0402-05
作者:
严静; 陈俊; 艾志兵; 周岗; 丁立; 何国厚
442000 湖北省十堰市湖北医药学院附属太和医院神经内科
Author(s):
Yan Jing; Chen Jun; Ai Zhibing; et al.
Department of Neurology,Taihe Hospital Affiliated to Hubei University of Medicine,Shiyan 442000
关键词:
可溶性环氧化物水解酶抑制剂 颈动脉狭窄 内皮祖细胞 PI3K/Akt信号通路
Keywords:
Soluble epoxide hydrolase inhibitor Carotid Stenosis Endothelial progenitor cell PI3K /Akt signaling pathway
分类号:
R543.5
DOI:
10.3969/j.issn.1007-0478.2017.05.005
摘要:
目的 探讨可溶性环氧化物水解酶抑制剂(sEHi)AUDA 调控颈动脉狭窄(CS)患者外周血内皮祖细胞(EPCs)增殖的分子机制。方法 从CS患者外周血分离、培养内皮祖细胞,收集培养至第7 d的细胞,分为未处理组、AUDA组、PI3K抑制剂(LY294002)组和AUDA+ LY294002组,取无颈动脉狭窄患者的EPCs作为对照组,MTT法检测EPCs的增殖能力,Western blot法检测EPCs Akt磷酸化的水平。结果 对照组EPCs增殖能力较未处理组增强,AUDA组较未处理组、AUDA+ LY294002组、LY294002组EPCs增殖能力增强,未处理组、AUDA+ LY294002组较LY294002组内皮祖细胞增殖能力增强; Western blot结果显示AUDA可以促进EPCs P-Akt蛋白的表达,而LY294002可以抑制上述作用。结论 AUDA可能通过活化PI3K /Akt信号通路来促进内皮祖细胞的增殖。
Abstract:
ObjectiveTo investigate the molecular mechanism of the soluble epoxide hydrolase inhibitor(sEHi)12-(3-adamantan-1-y1-ureido)-dodecagon acid(AUDA)in regulating the proliferation of endothelial progenitor cells(EPCs)in patients with carotid artery stenosis(CS).Methods EPCs were isolated and cultured from the peripheral blood of CS patients,cells were collected after 7 days of culture in vitro,and all of them were divided into Untreated group,AUDA group,PI3K inhibitor LY294002 group and AUDA+ LY294002 group.The proliferation of EPCs was determined by MTT,while the expression of phosphorylated Akt in EPCs was measured by Western blot.EPCs from people without carotid artery stenosis were also cultured as the controls.Results The proliferation of EPCs was stronger in the AUDA group than that in the untreated group,LY294002 group and AUDA+ LY294002 group,and the proliferation of EPCs was stronger in the untreated group and AUDA+ LY294002 group than that in the LY294002 group.Moreover,AUDA treatment increased phosphorylation of Akt,LY294002 which also blocked these effects.Conclusion The results of the present study suggested that AUDA promoted EPCs proliferation was related to the PI3K/Akt pathway.

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更新日期/Last Update: 2017-10-20