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克罗辛通过选择性向MKK4减弱了阻塞性病中Nrf2/GPX4介导的铁死

Ziyun Xu^1,2,3, Liwei Zhu^1,2, Jingyi Wu^1,2

¹Translational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, Jiangsu, China.

Phytotherapy research : PTR

|September 17, 2025

概括

沙弗朗中的一种化合物克罗辛通过抑制铁和纤维化来保护脏. 它向-MKK4 / Nrf2通路,显示作为脏疾病的脏保护剂的承诺.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
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:

纤维化是慢性病 (CKD) 发病的一个关键因素.
沙弗朗中的克罗辛已经显示出抗氧化和脏保护作用,但其在纤维化和铁化中的机制尚不清楚.

研究的目的:

研究crocin在保护细胞免受ferroptosis和改善纤维化的作用.
阐明克罗辛的脏保护作用背后的分子机制.

主要方法:

在NRK-52E细胞中利用单边尿路阻塞 (UUO) 鼠标模型和埃拉斯诱导的铁亡模型.
采用特异性抗体微阵列,表面等离子体共振 (SPR) 和共免疫沉 (Co-IP) 进行机制分析.

主要成果:

克罗辛减弱的纤维化和抑制的ferroptosis在体内和体外.
克罗辛与MKK4直接相互作用,抑制p-MKK4,然后与Nrf2相互作用,减少ROS和铁亡.
确定MKK4作为铁和纤维化的关键调节剂.

结论:

克罗辛通过调节-MKK4/Nrf2/ferroptosis信号轴来保护纤维化和铁化.
克罗辛是纤维化潜在的保护剂,MKK4是损伤相关损伤的治疗标.

关键词:

MKK4 MKK4 在线播放克罗辛克罗辛克罗辛克罗辛克罗辛克克罗辛克罗辛克克罗辛克铁性化 (ferroptosis) 是一种氧化应激是一种氧化应激.脏纤维化脏纤维化

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