食品科学 ›› 2011, Vol. 32 ›› Issue (15): 277-280.doi: 10.7506/spkx1002-6630-201115061

• 营养卫生 • 上一篇    下一篇

Trans C18:1通过NOS-NO系统诱导内皮细胞损伤研究

邱 斌,刘 蓉,邓泽元,*,范亚苇,李 静,胡蒋宁,黎 玉   

  1. 1.南昌大学 食品科学与技术国家重点实验室 2. 南昌大学生命科学与食品工程学院
  • 出版日期:2011-08-15 发布日期:2011-07-26
  • 基金资助:
    国家自然科学基金项目(30972482);江西省学术带头人计划项目(2008DD00900); 教育部博士点基金项目(20070403002);江西省自然科学基金项目(2008GQY0023)

trans C18:1-induced HUVEC Endotheliocyte Damage by NOS-NO System

QIU Bin1,LIU Rong1,DENG Ze-yuan1,*,FAN Ya-wei1,LI Jing1,HU Jiang-ning1,LI Yu2   

  1. (1. State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China; 2. School of Life Sciences and Food Engineering, Nanchang University, Nanchang 330047, China)
  • Online:2011-08-15 Published:2011-07-26

摘要: 为了观察trans C18:1对人脐静脉内皮细胞损伤的影响及其与NOS-NO系统的关系,首先将不同浓度trans C18:1 (50、100、200、400μmol/L)与人脐静脉内皮细胞共培养24或48h后,MTT法检测细胞存活率;用trans C18:1(200μmol/L)处理内皮细胞24h后,分别检测一氧化氮含量(NO)及一氧化氮合酶(NOS)活性;将trans C18:1与一氧化氮合酶阻断剂亚硝酸左旋精氨酸甲酯(LNAME)及一氧化氮供体(SNP)单一或联合处理内皮细胞,检测细胞存活率的变化。结果显示:trans C18:1以剂量和时间依赖方式导致内皮细胞的存活率下降; LNAME与trans C18:1联合处理内皮细胞后细胞存活率下降,而SNP与trans C18:1联合处理后细胞存活率上升;trans C18:1可诱导NO水平和内皮型一氧化氮合酶(eNOS)活性显著下降,而诱导型一氧化氮合酶(iNOS)活性无显著改变。表明:trans C18:1能通过抑制eNOS活性减少NO的分泌,并暗示NOS-NO系统可能是trans C18:1诱导内皮细胞损伤的作用机制之一。

关键词: NO, trans C18:1, 人脐静脉内皮细胞, NOS, 损伤

Abstract: In order to explore the mechanism of trans C18:1-induced endotheliocyte damage by NOS-NO system, the viability of human umbilical vein endothelial cells (HUVECs) subjected to trans C18:1 treatments at the concentrations of 50, 100, 200μmol/L and 400μmol/L for 24 or 48 h was determined by MTT assay. Meanwhile, the content of NO and the activity of NOS in HUVECs treated with trans C18:1 at the dose of 200μmol/L for 24 h were also determined using a commercial kit. Moreover, the viability of HUVECs subjected to treatments of trans C18:1 coupled with nitric oxide synthase inhibitor L-arginine methyl nitrite (LNAME) and/or nitric oxide donor (SNP) were also determined. The results indicated that trans C18:1 could decrease the viability of HUVECs in a dose- and time-dependent manner. The viability of HUVECs could be decreased by the combinatorial treatment of LNAME and trans C18:1 but increased by the combinatorial treatment of SNP and trans C18:1. trans C18:1 treatment could induce the secretion of NO and significantly decrease the activity of eNOS, but had no obvious effect on the activity of iNOS in HUVECs. Therefore, trans C18:1 treatment can reduce the secretion of NO through inhibiting eNOS activity, which suggests that the involvement of NOS-NO system is one of the important mechanisms of trans C18:1-induced HUVEC damage.

Key words: trans C18:1, human umbilical vein endothelial cell (HUVEC), NOS, NO, damage

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