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非致命的声动疗可以通过PI3K/AKT/mTORC1-自途径缓解高血压纤维化

DanDan Liu¹, Hui Wang¹, Jialong Li²

¹Department of Cardiology, The First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, 150001, PR China.

Scientific reports

|February 6, 2025

概括

非致命的声动疗法 (NL-SDT) 通过通过PI3K/AKT/mTORC1通路促进自,有效降低高血压纤维化. 这种新的非侵入性方法对治疗脏疾病和预防末期脏疾病 (ESRD) 是有前途的.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
生物医学工程生物医学工程
细胞生物学细胞生物学

背景情况:

高血压是末期病 (ESRD) 的主要原因,高血压病和纤维化是主要的并发症.
自对细胞健康和防治纤维化至关重要;其缺乏会加剧损伤和纤维化.
目前对高血压纤维化的治疗方法有限,这凸显了对新型治疗策略的需求.

研究的目的:

研究非致死性声动疗 (NL-SDT) 在抑制高血压纤维化方面的疗效.
阐明NL-SDT在调节纤维化中的潜在机制,重点关注自和相关信号通路.

主要方法:

一个小鼠模型的高血压纤维化被诱导使用血管素-II (Ang II) 输液.
每周使用NL-SDT,其中包括超声波激活声敏化剂 (sinoporphyrin) 来产生活性氧物种 (ROS).
纤维化通过马森三色染色和α-SMA表达;自标志物 (LC3B),信号蛋白 (PI3K/AKT/mTORC1) 和ROS水平通过西式抹染和其他测试来量化. 在体外研究中使用了TGF-β1诱导的NRK-52E细胞.

主要成果:

在高血压小鼠脏中,NL-SDT显著降低了原沉积和α-SMA表达.
治疗增加了自标志物LC3B的表达,并由自抑制剂 (拉帕米辛,CQ) 调节.
在体外,NL-SDT增加了ROS和自细胞,抑制了表皮-介质细胞转换 (EMT) 标记物,并降低了PI3K/AKT/mTORC1信号,表明自细胞的通路激活.

结论:

在高血压的小鼠模型中,NL-SDT通过抑制PI3K-AKT-mTORC1信号通路来促进自,有效地减轻纤维化.
作为高血压纤维化治疗的非侵入性和有效的治疗方法,NL-SDT显示出潜在的潜力,可能会延迟或预防ESRD.

关键词:

自自是一种自的过程.在EMT中,EMT是EMT.纤维化纤维化纤维化过高血压性脏病的发生.在NL-SDTT中使用.这就是PI3K-AKT-mTORC1的意思.

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