| 氯沙坦保护ox-LDL诱导的内皮细胞损伤与ADMA的关系 |
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| 引用本文： | 谢启应,孙泽琳,陈美芳,杨天(山仑). 氯沙坦保护ox-LDL诱导的内皮细胞损伤与ADMA的关系[J]. 中南大学学报(医学版), 2006, 31(1): 66-69 |
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| 作者姓名： | 谢启应 孙泽琳 陈美芳 杨天(山仑) |
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| 作者单位： | 中南大学湘雅医院心血管内科,长沙,410008;中南大学湘雅医院心血管内科,长沙,410008;中南大学湘雅医院心血管内科,长沙,410008;中南大学湘雅医院心血管内科,长沙,410008 |
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| 摘 要： | 目的：探讨氯沙坦对氧化型低密度脂蛋白（ox-LDL）诱导的内皮细胞损伤的保护作用及其与内源性一氧化氮合酶抑制物非对称性二甲基精氨酸（ADMA）的关系。方法：用ox-LDL（100mg／L）孵育人脐静脉内皮细胞株HUVEC12 24h或用10^-8～10^-6mmol／L的氯沙坦预孵育HUVEC12 30min后再与ox-LDL共孵育24h，测定培养液中乳酸脱氢酶（LDH）活性、一氧化氮（NO）、肿瘤坏死因子-α（TNF-α）、ADMA含量和细胞内二甲基精氨酸二甲胺水解酶（DDAH）活性。结果ox-LDL孵育HUVEC12细胞24h后细胞培养液中LDH活性、TNF-α和ADMA含量明显增加（P〈0．05），同时NO含量下降和细胞DDAH酶活性受到抑制（P〈0．05）；氯沙坦（10^-8～10^-6mmoL／L）可显著减轻ox-LDL诱导的LDH活性、TNF-α和ADMA含量的增加以及NO含量的降低（P〈0．05），并呈浓度依赖性的增加DDAH活性（P〈0.05）。结论：氯沙坦对ox-LDL诱导的血管内皮细胞损伤具有保护作用，该作用可能与增加DDAH活性，降低ADMA浓度有关。
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| 关 键 词： | 氯沙坦 内皮细胞 氧化型低密度脂蛋白 非对称性二甲基精氨酸 二甲基精氨酸二甲胺水解酶 |
| 文章编号： | 1672-7347（2006）01-0066-04 |
| 收稿时间： | 2005-06-27 |
| 修稿时间： | 2005-06-27 |
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| XIE Qi-ying,SUN Ze-lin,CHEN Mei-fang,YANG Tian-lun.
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| Authors: | XIE Qi-ying SUN Ze-lin CHEN Mei-fang YANG Tian-lun |
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| Affiliation: | Department of Cardiolog, Xiangya Hospital, Central Soutth University, Changsha 410008, China. |
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| Abstract: | OBJECTIVE: To investigate the protective effect of losartan against on injury induced by ox-LDL in endothelial cells and the relationship with asymmetric dimethylarginine (ADMA). METHODS: Endothelial injury was induced by incubation with ox-LDL 100 mg/L in cultured HUVECs for 24 h, and the levels of ADMA, lactate dehydrogenase (LDH), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) in the conditioned medium were measured. The activity of dimethylarginine dimethylaminohydrolase (DDAH) of cultured endothelial cells was also determined. RESULTS: Incubation of endothelial cells with ox-LDL 100 mg/L for 24 h induced a marked elevation of the levels of ADMA, LDH and TNF-alpha in the conditioned medium and a significant decrease in the activity of DDAH and the content of NO (P < 0.05). Pretreatment with losartan (10(-8) - 10(-6) mmol/L) significantly inhibited the increased levels of ADMA, LDH and TNF-alpha, attenuated the decreased levels of NO and the decreased activity of DDAH induced by ox-LDL (P < 0.05). CONCLUSION: Losartan may preserve ox-LDL-induced endothelial cell injury by increasing the DDAH activity and decreasing the ADMA level. |
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| Keywords: | losartan endothelial cells oxidative low-density lipoprotein asymmetric dimethylarginine dimethylarginine dimethylaminohydrolase |
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