Analysis of cardiovascular complications by the production of reactive oxygen species from mitochondria in patients with glucocrticoid excess
糖皮质激素过量患者线粒体产生活性氧引起的心血管并发症分析
基本信息
- 批准号:10670663
- 负责人:
- 金额:$ 2.11万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1998
- 资助国家:日本
- 起止时间:1998 至 1999
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The effect of glucbcrticoid excess on the production of reactive oxygen species (ROS), peroxynitrate and nitric oxide (NO) was investigated using the fluorescence probe (CM-HィイD22ィエD2DCFDA, DHR123 and DAF-2) in cultured human vascular endothelial cells from umbilical cord vein (HUVEO). The productions of ROS and peroxynitrate were significantly increased, but the production of NO was significantly decreased in 10ィイD1-7ィエD1M dexamethasone-treated HUVEC. Western blot analysis of 3-nitrotyrosine (foot print of peroxynitrate) showed increase of peroxynitrate in dexamethasone-treated HUVEC. Over-production by glucocorticoid excess was markedly suppressed by carbonyl cyanide m-chlorophenylhyazone, which could decrease ROS production from mitochondrial respiratory chain. Furthermore, the inhibition of complex I by diphenyleneiodinium chloride and the inhibition of complex 11 by thenoyltrifluoroadetone significantly decrease the over-production of ROS in dexamethasone-treated HLVEC. However, the inhibition of complex 111 by myxothiazol could not decrease the over-production of ROS in dexamethasone-treated HUVEC.These findings showed that glucoeorticoid excess could cause the over-production of ROS from complex I and II in mitochondrial respiratory chain, and subsequently the consumption of NO in vascular endothekial cells. The production of ROS and consumption of NO by glucocorticoid excess could impair the vascular endothelial function, which may be a major pathogenesis for cardiovascular complications in patients with glucocorticoid excess.
用荧光探针(CM-H荧光素D22荧光素D2 DCFDA、DHR 123和DHR 123)研究了糖皮质激素过量对培养的人脐静脉血管内皮细胞(HUVEO)产生活性氧(ROS)、过氧硝酸盐(过氧硝酸盐)和一氧化氮(NO)的影响。10 μ mol/L D1-7 μ mol/L D1 M地塞米松处理HUVEC后,ROS和过氧硝酸盐的产生显著增加,而NO的产生显著减少。3-硝基酪氨酸(过氧硝酸盐足迹)的蛋白质印迹分析显示地塞米松处理的HUVEC中过氧硝酸盐增加。碳酰氰间氯苯腙能显著抑制糖皮质激素过量引起的线粒体呼吸链活性氧的产生。此外,抑制复合物I由diphenyleniodinium氯化物和抑制复合物11由thenoyltrifluoroadetone显着减少过量生产的活性氧在地塞米松处理的HLVEC。而Myxothiazol对复合物111的抑制作用并不能降低地塞米松处理的HUVEC中ROS的过量产生,提示糖皮质激素过量可导致线粒体呼吸链复合物I和II的ROS过量产生,进而导致血管内皮细胞对NO的消耗。糖皮质激素过量引起的ROS产生和NO消耗,可损害血管内皮功能,这可能是糖皮质激素过量患者心血管并发症的主要发病机制之一。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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AKAIKE Masashi其他文献
AKAIKE Masashi的其他文献
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{{ truncateString('AKAIKE Masashi', 18)}}的其他基金
Development of training program introducing clinical clerkship to acquire 360 degree communication skills and abilities
制定临床实习培训计划,以获取 360 度沟通技巧和能力
- 批准号:
15K08554 - 财政年份:2015
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Glucocorticoid-induced vascular endothelial dysfunction through activation of mineralcorticoid receptor
糖皮质激素通过激活盐皮质激素受体诱导血管内皮功能障碍
- 批准号:
21590955 - 财政年份:2009
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$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
A novel therapeutic strategy for glucocorticoid-induced vascula endothelial dysfundtion
糖皮质激素引起的血管内皮功能障碍的新治疗策略
- 批准号:
19590866 - 财政年份:2007
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Novel regulatory mechanism of vascular endothelial function mediated by BMK1/ERK5 and its application for anti-atherosclerosis therapy
BMK1/ERK5介导的血管内皮功能调控新机制及其在抗动脉粥样硬化治疗中的应用
- 批准号:
17590740 - 财政年份:2005
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Thrombin-induoed vascular injury through the overproduction of reactive oxygen species
活性氧过量产生凝血酶引起的血管损伤
- 批准号:
12670674 - 财政年份:2000
- 资助金额:
$ 2.11万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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