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氨酸通过MAPK/TGF-β1/Smad2/3信号传递改善AngII诱导的血管改造

Peizhi Jia¹, Daxin Chen², Ying Zhu³

¹Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.

Journal of ethnopharmacology

|June 12, 2023

概括

氨酸 (Lien) 通过保护血管有效治疗高血压. 这种类化合物抑制了血管重塑,为开发抗高血压疗法提供了新的途径.

科学领域:

药理学药理学是指药理学的学科.
心血管研究研究心血管研究
自然产品化学自然产品化学

背景情况:

氨酸 (Lien) 是plumula nelumbinis中的一种类化合物,具有抗高血压的特性.
在高血压中,Lien对目标器官的特定保护机制在很大程度上仍未被阐明.
了解Lien的血管保护对于开发新型抗高血压治疗至关重要.

研究的目的:

研究Lien在高血压治疗中的治疗作用背后的机制.
为了明确Lien在血管保护中对高血压损伤的作用.
探索Lien对血管改造通路的影响.

主要方法:

从plumula nelumbinis中提取和分离李恩.
在小鼠中建立Ang II诱导的高血压的体内模型.
评估血压,脉冲波速度和大动脉介质厚度.
在血管中进行差异基因和途径分析的RNA测序.
分子对接以确定Lien-MAPK相互作用.
血管重塑标记物 (PCNA,α-SMA,原I/III) 的组织学分析 (HE,Sirius红色染色) 和蛋白质表达分析 (IHC,西部斑).
使用MAPK通路调节器 (PD98059,TPA) 的体外研究证实了Lien的作用机制.

主要成果:

莱恩在高血压小鼠中表现出显著的抗高血压作用,降低血压和大动脉血管重塑.
RNA测序揭示了Lien逆转了与高血压相关的差异性基因表达途径,特别是与增殖相关的途径.
莱恩抑制了Ang II诱导的MAPK/TGF-β1/Smad2/3信号通路的激活,减少了原沉积,并防止了血管重塑.
在体外实验证实了Lien能够抵消Ang II诱导的TGF-β1和α-SMA表达的变化,这种变化通过MAPK途径进行介导.

结论:

莱恩通过抑制血管重塑,对高血压产生保护作用.
该机制涉及对MAPK/TGF-β1/Smad2/3信号通路的调制.
作为高血压的治疗剂,Lien显示出前景,为开发新的抗高血压药物提供了基础.

关键词:

血管新生素II的产生高血压血管改造高血压血管改造氨酸是一种氨酸.这就是MAPKK的意思.在TGF-β1/Smad2/3/3中.

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