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。
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.
出处
《食品科学》
EI
CAS
CSCD
北大核心
2011年第15期277-280,共4页
Food Science
基金
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)
