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作 者:邱斌[1] 刘蓉[1] 邓泽元[1] 范亚苇[1] 李静[1] 胡蒋宁[1] 黎玉[2]
机构地区:[1]南昌大学食品科学与技术国家重点实验室,江西南昌330047 [2]南昌大学生命科学与食品工程学院,江西南昌330047
出 处:《食品科学》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)
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.
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