脑下垂体副腹腔核中的神经Sik1降低了高盐饮食后的血压升高
Wei Zhang1,2, Ping Wang1,2,3,4, Shuya Qi1,2
1Institute of Neuroscience and Guangxi Key Laboratory of Brain Science, Department of Human Anatomy, School of Basic Medical Sciences, Guangxi Medical University, 22 Shuang-Yong Road, Nanning, Guangxi, 530021, People's Republic of China.
在大脑的副腹腔核 (PVN) 中的神经Sik1对于调节血压至关重要. 它的缺失会通过影响NF-κB通路和增加炎症而加剧对盐敏感高血压.
科学领域:
- 神经科学是一个神经科学.
- 心血管生理学心血管生理学
- 分子生物学分子生物学
背景情况:
- 血压调节是复杂的,涉及大脑与器官的相互作用.
- 脑下垂体副心脏核 (PVN) 是控制血压的关键.
- 在盐敏感高血压中PVN的作用尚未完全理解.
研究的目的:
- 调查PVN中Sik1在调节盐敏感高血压中的作用.
- 阐明Sik1在高血压中的功能背后的分子机制.
主要方法:
- 使用了淘汰赛小鼠模型 (Sik1淘汰赛,Nestin-Cre;Sik1-/-).
- 在PVN神经元中采用了AAV-Cre介导的基因删除.
- 进行了西部斑点,免疫光和单核RNA测序.
- 进行了KEGG路径分析.
主要成果:
- 在高盐饮食 (HSD) 下,PVN神经元中Sik1的升高调节.
- 在PVN神经元中Sik1的消去导致血压升高,以应对HSD.
- Sik1 缺陷降低了NF-κB 途径的调节,并激活了表达阿尔金因血管压素 (AVP) 的 PVN 神经元中的微质.
结论:
- 在AVP阳性PVN神经元中的神经元Sik1减弱了HSD诱导的血压升高.
- Sik1可以通过对NF-κB信号通路的调制来发挥作用.
- 神经元Sik1在对盐敏感高血压的病理生理学中发挥着新的作用.
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