在下丘脑副腹腔核中激活AMPK通过ERK1/2-NF-κB通路改善再生血管高血压
Li-Yan Fu1, Yu Yang1,2, Rui-Juan Li3
1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center; Institute of Cardiovascular Sciences, Translational Medicine Institute, Xi'an Jiaotong University Health Science Center; Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education, Xi'an, 710061, Shaanxi, China.
Cardiovascular toxicology
|July 15, 2024
概括
在大脑中AMP激活蛋白激酶 (AMPK) 的激活.
科学领域:
- 神经科学是一个神经科学.
- 心血管研究研究心血管研究
- 代谢信号传递 代谢信号传递
背景情况:
- 高血压的发病过程很复杂,机制不清楚.
- AMP激活蛋白激酶 (AMPK) 影响能量代谢和高血压.
- 之前的研究结果显示,高血压大鼠大脑中AMPK,AT1-R和ERK1/2的变化.
研究的目的:
- 研究AMPK调节血管新素II类型1受体 (AT1-R) 的机制,通过对腹腔核 (PVN) 中的ERK1/2-NF-κB通路进行调节.
- 为了确定PVN中的AMPK激活是否抑制了交感神经活动并改善了高血压.
主要方法:
- 采用了一种两,一 (2K1C) 血管高血压的老鼠模型.
- 在小鼠的PVN中微注射AICAR (AMPK激活剂) 或载体4周.
- 测量了缩血压 (SBP),上腺素 (NE),以及p-AMPK,AT1-R,p-ERK1/2和NF-κB p65.5的蛋白质表达/活性.
主要成果:
- 2K1C大鼠表现出增加的SBP,NE,p-ERK1/2,AT1-R和NF-κB p65活性,p-AMPK降低.
- 在2K1C大鼠中,AICAR治疗降低了SBP,NE,p-ERK1/2,AT1-R和NF-κB p65活性.
- 在2K1C大鼠的PVN中,AICAR治疗增加了p-AMPK水平.
结论:
- 在PVN中的AMPK激活通过抑制ERK1/2-NF-κB通路来抑制AT1-R表达.
- 这种机制降低了同情神经系统的活动.
- 在PVN中的AMPK激活在血管模型中改善了高血压.
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