沈千万通过上调AQP1来减轻脏间歇性纤维化
Yiyou Lin1, Jiale Wei1, Yehui Zhang1
1School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Chinese journal of natural medicines
|May 28, 2023
概括
沈奇万 (SQW) 通过上调水素1 (AQP1) 的调节,缓解脏间歇性纤维化 (RIF),抑制管状上皮细胞转化为介质细胞转化 (EMT). 这项研究澄清了SQW.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 间纤维化 (RIF) 是慢性病 (CKD) 进展到末期功能衰竭的关键过程.
- 传统中医药的治疗机制,如Shen Qi Wan (SQW),在缓解RIF方面仍然不完全理解.
- 管状上皮细胞转变为介质细胞 (EMT) 是一个关键的细胞事件,有助于RIF.
研究的目的:
- 调查水素1 (AQP1) 在SQW对RIF和EMT的保护作用中的作用.
- 阐明SQW影响EMT的分子机制,重点关注AQP1表达.
- 评估SQW在改善既定模型中的损伤和纤维化方面的疗效.
主要方法:
- 在小鼠中确定的腺因诱导的RIF和转化生长因子β1 (TGF-β1) 刺激的HK-2细胞模型用于体外和体外研究.
- 在HK-2细胞中利用了AQP1的淘汰,以探索其在SQW的作用机制中的特定作用.
- 通过分子和组织学技术评估损伤,原沉积和关键EMT标记物的表达 (E-cadherin,vimentin,α-平滑肌肉动蛋白,牛,牛,CK-18).
主要成果:
- 在腺因诱导的RIF小鼠中,SQW治疗显著降低了损伤和原沉积.
- 在体内,SQW上调调节了E-cadherin和AQP1的表达,同时降低了维门丁和α-平滑肌肉动蛋白 (α-SMA) 的调节.
- 在HK-2细胞中,SQW抑制了TGF-β1诱导的EMT,这种效果取决于AQP1的表达,因为AQP1的淘汰促进了EMT并取消了SQW的保护作用.
结论:
- SQW通过减弱管状上皮质到介质酶过渡,对脏间歇性纤维化产生保护作用.
- 该机制涉及水素1 (AQP1) 表达的上调,这对于SQW的抗纤维素和抗EMT作用至关重要.
- 这些发现突出了AQP1作为一种潜在的治疗点,用于管理SQW的CKD进展.
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