...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >High glucose increases expression of cyclooxygenase-2, increases oxidative stress and decreases the generation of nitric oxide in mouse microvessel endothelial cells.
【24h】

High glucose increases expression of cyclooxygenase-2, increases oxidative stress and decreases the generation of nitric oxide in mouse microvessel endothelial cells.

机译：高葡萄糖增加的表达cyclooxygenase-2,增加氧化应激在鼠标减少一氧化氮的生成微血管内皮细胞。

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

Hyperglycaemia is a key factor that contributes to the development of diabetes-related microvascular disease. Both cyclooxygenase I and cyclooxygenase II are expressed in endothelial cells and play key roles in the regulation of cardiovascular function. In the current study we tested the hypothesis that hyperglycaemia-induced increased expression of cyclooxygenase II is a contributing factor both to the increased oxidative stress and to the reduction in the generation of nitric oxide in microvessel endothelial cells following their exposure to high glucose. We demonstrated that the exposure of mouse microvascular endothelial cells to high glucose for 3 days decreased the generation of nitric oxide and enhanced production of superoxide. Western blots illustrated that exposure to high glucose also increased endothelial nitric oxide synthase and cyclooxygenase II protein expression levels and decreased the dimer/monomer ratio of endothelial nitric oxide synthase protein. All the changes induced by the high glucose culture media could be reversed by either the cyclooxygenase II inhibitor CAY10404, the non-selective cyclooxygenase inhibitor indomethacin or the protein kinase C inhibitor chelerythrine, but not solely by preincubation with the antioxidant and putative NADPH oxidase inhibitor, apocynin. Our data indicate that high glucose induced oxidative stress is linked to an increase in the expression of cyclooxygenase II and a reduced generation of nitric oxide that is associated with an uncoupled endothelial nitric oxide synthase, possibly due to decreased dimer/monomer ratio.
机译：导致高血糖症是一个关键因素糖尿病的微血管的发展疾病。二世在内皮细胞表达和玩耍调节心血管的关键角色函数。假设hyperglycaemia-induced增加表达式的环氧酶II是一种贡献增加氧化应激和因素减少氮的生成氧化后微血管内皮细胞他们暴露于高葡萄糖。的接触鼠标微血管内皮细胞高葡萄糖3天一氧化氮的生成和减少增强超氧化物的生产。说明暴露在高葡萄糖增加内皮一氧化氮合酶和环氧酶2蛋白表达水平内皮的二聚体/单体比率下降一氧化氮合酶蛋白质。诱导的高葡萄糖培养基通过环氧酶II被逆转抑制剂CAY10404,无选择性环氧酶抑制剂消炎痛或蛋白激酶C抑制剂白屈菜赤碱,但不是仅仅通过预培养和抗氧化剂假定的NADPH氧化酶抑制剂,apocynin。数据表明,高葡萄糖诱导氧化压力是与增加表达式环氧酶II和减少一代一氧化氮与非耦合相关联内皮一氧化氮合酶,可能是因为二聚体/单体比率下降。

著录项

相似文献

  • 外文文献
  • 中文文献
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