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酸精酸盐B通过调节KLF5/CDK1/Cyclin B1通路来防止缺血性AKI-to-CKD进展

Liyu Lin¹, Daoqi Shen², Yiqi Su¹

¹Department of Nephrology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, PR China; Xiamen Clinical Quality Control Center of Nephrology, Xiamen, 361015, PR China.

Phytomedicine : international journal of phytotherapy and phytopharmacology

|April 22, 2025

概括

石精B (Mlb) 通过调节细胞循环进展,缓解急性损伤 (AKI) 后的纤维化. 这种化合物向KLF5/CDK1/Cyclin B1通路,具有预防慢性病 (CKD) 进展的潜力.

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.
分子生物学分子生物学

背景情况:

缺血-再输液损伤 (IRI) 是急性损伤 (AKI) 的主要原因,经常发展为慢性病 (CKD) 和纤维化.
来自Salvia miltiorrhiza Bunge的石精B (Mlb) 显示出保护脏免受AKI的承诺,但其在AKI-CKD过渡和抗纤维机制中的作用尚不清楚.

研究的目的:

研究Mlb对AKI向CKD进展的治疗效果.
阐明MLB抗纤维素活性的潜在机制,重点关注细胞循环调节.

主要方法:

使用单边缺血/再输 (UIR) 诱导的AKI-to-CKD小鼠模型 (体内) 和HK-2细胞中TGF-β诱导的纤维化 (体内).
采用组织学分析,分子分析,网络药理学和RNA测序来评估纤维化和细胞循环途径.

主要成果:

Mlb治疗改善了小鼠在UIR后诱导的AKI中的功能,减少了炎症,亡和G2/M阶段细胞周期停止,从而改善了纤维化.
Mlb增强了CDK1/Cyclin B1通路活性,缓解了细胞周期停滞. 网络药理学和RNA测序确定了KLF5/CDK1/Cyclin B1作为一个关键的MLB标途径.
用ML264抑制KLF5逆转了Mlb的保护作用,证实了该通路在Mlb介导的保护中的关键作用.

结论:

在AKI-to-CKD进展过程中,MLB有效地减少纤维化,通过KLF5/CDK1/Cyclin B1信号通路抑制G2/M阶段细胞周期停止.
这些发现突显了Mlb在预防AKI后CKD的治疗潜力,并揭示了涉及KLF5/CDK1/Cyclin B1通路的新机制.

关键词:

从AKI到CKD的进展情况急性损伤是什么?急性损伤是什么?在KLF5 5KLF5 石精乙酸乙酸是什么意思患有脏纤维化细胞周期停滞细胞周期停滞

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