• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Endothelium: Journal of endothelial cell research >Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells.
【24h】

Effect of homocysteine on nitric oxide production in coronary microvascular endothelial cells.

机译：同型半胱氨酸对冠状微血管内皮细胞中一氧化氮产生的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hyperhomocysteinemia is widely recognized as an independent risk factor for coronary artery vascular disease, although the underlying mechanisms are not well understood. This study aims to investigate the effect of homocysteine on nitric oxide (NO) production in coronary microvascular endothelial cells (CMECs) and putative mechanisms mediating this effect. CMECs were isolated on Langendorff system by collagenase perfusion of hearts from male rats and cultured. The effect of homocysteine (0.01 to 1 mM) on basal and stimulated NO production was evaluated by measuring nitrite in the culture media after incubation with or without N(G)-nitro-L-arginine methyl ester (L-NAME) (1 mM), superoxide dismutase (100 U/mL), or catalase (1000 U/mL) for 24 h. Total nitrite was measured using Griess reaction after reduction of nitrate to nitrite with nitrate reductase. Homocysteine did not affect basal nitrite accumulation; however, it significantly increased the nitrite accumulation induced by the calcium ionophore A23187 or interleukin-1beta only at 1 mM. This effect of homocysteine was significantly inhibited by L-NAME, superoxide dismutase, and catalase. In conclusion, homocysteine increases NO release from stimulated CMECs without affecting basal NO production, which is probably accompanied by increased production of reactive oxygen species. It can be postulated that endothelial cells generate NO in order to minimize the damage caused by homocysteine.
机译：高同型半胱氨酸血症被广泛认为是冠状动脉血管疾病的独立危险因素，尽管其潜在机制尚不清楚。这项研究旨在调查高半胱氨酸对冠状微血管内皮细胞（CMEC）中一氧化氮（NO）产生的影响，以及介导这种作用的推测机制。通过在雄性大鼠的心脏中进行胶原酶灌注，在Langendorff系统上分离CMEC，并进行培养。通过在有或没有N（G）-硝基-L-精氨酸甲酯（L-NAME）（1 mM）孵育后测量培养基中的亚硝酸盐来评估高半胱氨酸（0.01至1 mM）对基础和刺激NO产生的影响），超氧化物歧化酶（100 U / mL）或过氧化氢酶（1000 U / mL）处理24小时。使用硝酸还原酶将硝酸盐还原为亚硝酸盐后，使用Griess反应测量总亚硝酸盐。同型半胱氨酸不影响基础亚硝酸盐的积累;但是，它仅在1 mM时显着增加了钙离子载体A23187或白介素1β诱导的亚硝酸盐积累。高半胱氨酸的这种作用被L-NAME，超氧化物歧化酶和过氧化氢酶显着抑制。总之，高半胱氨酸增加了刺激的CMEC中NO的释放，而不会影响基础NO的产生，这可能伴随着活性氧的产生增加。可以推测内皮细胞产生NO，以最小化由同型半胱氨酸引起的损害。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号