[1]韩锡萍,张 鹏,于 凡,等.高盐抑制胸主动脉内皮细胞一氧化氮生成及其机制[J].中国药理学通报,2019,(09):1251-1256.[doi:10.3969/j.issn.1001-1978.2019.09.013]
 HAN Xi-ping,ZHANG Peng,YU Fan,et al.High salt inhibits nitric oxide production in thoracic aortic endothelial cells and its mechanism[J].Chinese Pharmacological Bulletin,2019,(09):1251-1256.[doi:10.3969/j.issn.1001-1978.2019.09.013]
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高盐抑制胸主动脉内皮细胞一氧化氮生成及其机制()
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《中国药理学通报》[ISSN:/CN:]

卷:
期数:
2019年09期
页码:
1251-1256
栏目:
论著
出版日期:
2019-09-09

文章信息/Info

Title:
High salt inhibits nitric oxide production in thoracic aortic endothelial cells and its mechanism
文章编号:
1001-1978(2019)09-1258-06
作者:
韩锡萍1张 鹏2于 凡2冯 磊2马 鑫2
江南大学1.药学院、2.无锡医学院,江苏 无锡 214122
Author(s):
HAN Xi-ping1 ZHANG Peng2 YU Fan2 FENG Lei2 MA Xin12
1.School of Pharmaceutical Sciences; 2.Wuxi School of Medicine, Jiangnan University,Wuxi Jiangsu 214122,China
关键词:
内皮细胞 高盐 TRPV4 一氧化氮 HC067047 Ca2+内流
Keywords:
endothelial cells high salt TRPV4 NO HC067047 Ca2+ influx
分类号:
R-332; R151.2; R322.121; R329.24; R348.1; R916.3
DOI:
10.3969/j.issn.1001-1978.2019.09.013
文献标志码:
A
摘要:
目的 探究小鼠胸主动脉内皮细胞高盐模型对一氧化氮(nitric oxide,NO)生成的影响。方法 使用瞬时受体电位香草素4(transient receptor potential vanilloid 4,TRPV4)抑制剂HC067047对胸主动脉内皮细胞预孵育后,通过钙离子荧光探针Fluo-4和NO荧光探针DAF-FM DA进行Ca2+以及NO标记,研究TRPV4对NO产生的影响。以60 mmol·L-1高盐刺激胸主动脉内皮细胞,检测Ca2+内流以及NO的生成情况。结果 与对照组相比,抑制TRPV4减少胸主动脉内皮细胞Ca2+内流及NO的生成; 与同渗透压的甘露醇相比,高盐抑制胸主动脉内皮细胞中TRPV4介导的Ca2+内流及NO的生成。结论 高盐状态下,通过抑制TRPV4通道导致Ca2+内流减少,NO的生成下降。
Abstract:
Aim To investigate the effect of high-salt model of mouse thoracic aortic endothelial cells on the production of nitric oxide(NO).Methods After pre-incubation of thoracic aortic endothelial cells with transient receptor potential vanilloid 4(TRPV4)inhibitor HC067047, the effects of TRPV4 on NO production were studied by Ca2+ and NO staining with calcium ion fluorescent probe Fluo-4 and NO fluorescent probe DAF-FM DA.The thoracic aortic endothelial cells were stimulated with a high salt concentration of 60 mmol·L-1 to detect Ca2+ influx and NO production.Results Compared with control group, suppression of TRPV4 inhibited Ca2+ influx and NO production in thoracic aortic endothelial cells, and high salt conditions inhibited TRPV4-medicated Ca2+ influx and NO production compared with mannitol under the same osmotic pressure.Conclusion In high salt state, the inhibition of TRPV4 channel leads to the decrease of Ca2+ influx and the down-regulation of NO synthesis.

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备注/Memo

备注/Memo:
收稿日期:2019-03-20,修回日期:2019-06-21
基金项目:国家自然科学基金资助项目(No 81700437)
作者简介:韩锡萍(1994-),女,硕士生,研究方向:分子药理学,E-mail:jiangnan6161504006@163.com;
马 鑫(1981-),男,博士,教授,研究方向:药理学,通讯作者,E-mail:maxin@jiangnan.edu.cn
更新日期/Last Update: 2019-08-14