在加速衰老的小鼠模型中,潜在的呼吸缺陷的中心和外周机制
Alembert Lino-Alvarado1, Octavio A C Maia2, Maria Aparecida Oliveira3
1Biomedical Engineering Laboratory, University of Sao Paulo, Sao Paulo, SP, Brazil.
Pflugers Archiv : European journal of physiology
|August 16, 2024
概括
小鼠加速衰老 (SAMP8) 通过减少神经素-1 (NK1) 受体神经元和改变呼吸机制,影响中枢和外围呼吸功能,损害呼吸控制.
科学领域:
- 神经科学是一个神经科学.
- 呼吸系统生理学 呼吸系统生理学
- 衰老研究研究 衰老研究
背景情况:
- 衰老会影响神经系统和呼吸控制.
- 衰老与呼吸功能之间的联系需要进一步研究.
- 衰老加速鼠标倾向8 (SAMP8) 模型加速了衰老.
研究的目的:
- 在加速衰老的小鼠模型 (SAMP8) 中调查呼吸系统异常.
- 评估SAMR8小鼠中与对照小鼠 (SAMR1) 相比的中心和外周呼吸功能.
主要方法:
- 整体囊造影以评估呼吸系统参数.
- 呼吸道输入阻抗测量.呼吸道输入阻抗测量.
- 针对神经素-1受体密度的免疫组织化学.
- 对低氧和高头的呼吸系统反应的评估.
- 测量呼吸机制和甲胆反应.
主要成果:
- SAMP8小鼠在腹腔呼吸柱中显示出神经基因素-1受体密度降低.
- 在SAMP8小鼠中观察到对缺氧和高头的减弱的太基普尼反应.
- 在SAMP8小鼠中注意到静态合规性,灵感能力,耐力和弹性降低.
- SAMP8小鼠对甲醇的收缩反应减弱.
结论:
- 在SAMP8小鼠中加速衰老与呼吸中心NK1表达神经元的损失有关.
- 在SAMP8小鼠中,中央和外周呼吸机制的损伤明显.
- 这些发现表明,衰老对这种动物模型中的呼吸控制有显著的影响.
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