c-Jun N-终端激酶2的缺乏可以防止高胆固醇血症引起的内皮功能障碍和氧化应激
Elena Osto1, Christian M Matter, Alexei Kouroedov
1Cardiology and Cardiovascular Research, Institute of Physiology, Zurich, Switzerland.
Circulation
|October 29, 2008
概括
删除JNK2可以防止高胆固醇引起的内皮功能障碍和氧化应激. 这表明JNK2是血管疾病和动脉样硬化发展的关键因素.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 氧化压力研究研究 氧化压力研究
背景情况:
- 高胆固醇血症通过内皮功能障碍和反应性氧物种 (ROS) 触发了以太基生成.
- 由氧化应激激活的c-Jun-N-终端激酶 (JNKs) 参与动脉生成和炎症.
研究的目的:
- 调查JNK2缺失是否能预防高胆固醇血症引起的内皮功能障碍和氧化应激.
主要方法:
- 雄性JNK2淘汰赛 (JNK2(-/-)) 和野生型 (WT) 鼠被食高胆固醇饮食 (HCD) 或正常饮食14周.
- 评估了依赖内皮和独立内皮的放松,氧化 (NO) 的释放以及内皮NO合成酶 (eNOS) 和抗氧化酶的表达.
主要成果:
- 在HCD的WT小鼠中,JNK酸化增加和内皮依赖放松功能受损.
- 患有HCD的JNK2(-/-) 小鼠没有表现出内皮功能障碍,保持了NO释放,并上调了eNOS表达.
- 在HCD上的WT小鼠增加了氧化应激标志物 (O(2) ((-),ONOO(-),尼托铁),与JNK2 ((-/-) 小鼠不同.
结论:
- JNK2是高胆固醇血引起的内皮功能障碍和氧化应激的关键调解者.
- 向JNK2可能为预防血管疾病和动脉样硬化提供一种新的治疗策略.
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