高血压压抑,但运动训练恢复Mfsd2a表达和PVN毛细血管内的血脑屏障功能
Sany M Perego1, Hiviny A Raquel1, Vanessa B Candido1
1Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, Brazil.
概括
运动训练通过增加Mfsd2a表达来使高血压大鼠的血脑屏障 (BBB) 功能正常化. 这种机制恢复了自主控制,并降低了BBB的透性,突出了炼.
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:
- 高血压增加了前自主区域的血脑屏障 (BBB) 转细胞,导致自主失衡.
- 关联高血压,BBB功能和自主控制的分子机制仍然不太清楚.
- Mfsd2a是多可萨赫萨酸 (DHA) 的关键载体,对BBB的完整性至关重要.
研究的目的:
- 调查Mfsd2a在高血压和运动诱导的BBB转细胞的变化中的作用.
- 确定运动训练是否可以恢复Mfsd2a的表达,并改善高血压大鼠的BBB功能和自主控制.
主要方法:
- 自发高血压大鼠 (SHR) 和Wistar大鼠接受了为期4周的跑步机训练或保持久坐.
- 血液动力学和自主性参数被测量在有意识的老鼠.
- 评估了下丘脑侧心膜核 (PVN) 中的BBB透性,并分析了Mfsd2a和caveolin-1表达水平.
主要成果:
- 与正常血压对照相比,高血压大鼠表现出增加的BBB透性,减少的Mfsd2a,以及高高的卡韦林-1表达.
- 在高血压大鼠中,运动训练使PVN BBB的透性正常化,增加了Mfsd2a密度,并减少了caveolin-1的表达.
- 在高血压大鼠中,训练也改善了自主参数,包括心率变化和巴罗反射控制.
结论:
- 运动训练有效地拯救了高血压大鼠的Mfsd2a表达,从而纠正了BBB功能障碍.
- 通过Mfsd2a介导的DHA传输到内皮细胞中,减少了卡韦林-1和囊泡的形成,使BBB的透性正常化.
- 运动诱导的Mfsd2a恢复是改善高血压中BBB功能和自主控制的关键机制.
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