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在脏急性管状缩中,加勒-3和自

Suhail Al-Salam¹, Govindan S Jagadeesh¹, Manjusha Sudhadevi¹

¹Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, Alain P.O. Box 15551, United Arab Emirates.

International journal of molecular sciences

|April 13, 2024

概括

盖莱克-3 (Gal-3) 缺乏会增强西斯普拉丁诱导的急性损伤 (AKI) 的自. 这项研究揭示了Gal-3

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
细胞生物学细胞生物学
在瘤学瘤学.

背景情况:

急性损伤 (AKI),通常是由急性管状缩 (ATN) 引起的,是一个重大的健康问题.
化疗药物西斯普拉丁 (CIS) 是ATN的常见诱导剂.
自与AKI有关,在AKI中加勒-3 (Gal-3) 含量升高,但其在自中的作用尚不清楚.

研究的目的:

调查加勒-3 (Gal-3) 在西斯普拉丁诱导的急性损伤 (ATN) 过程中自的作用.

主要方法:

在野生类型和Gal-3淘汰赛小鼠中使用了一种cisplatin小鼠ATN模型.
使用组织学,免疫光学和ELISA评估Gal-3和与自相关的蛋白质的表达.
分析的蛋白质度包括LC3B,ATG13,Ulk-1,Beclin,ATG5,ATG12,ATG9A,p-AMPK,mTOR,p-NF-κB,β-catenin,以及p62. 这些蛋白质的度是:

主要成果:

在野生型小鼠中,西斯普拉丁治疗显著增加了脏Gal-3.
在暴露于西斯后,与野生类型小鼠相比,Gal-3淘汰赛小鼠表现出更高水平的自蛋白 (LC3B,ATG13,Ulk-1,Beclin,ATG5,ATG12,ATG9A,p-AMPK).
野生类型小鼠的mTOR,p-NF-κB,β-catenin和p62度较高,与Gal-3淘汰赛小鼠相比.

结论:

加勒-3 (Gal-3) 在 AKI 中在调节细胞反应和生存信号通路方面发挥着至关重要的作用.
缺少Gal-3可以增强自性,而在西斯普拉丁诱导的ATN的背景下.
-3与自蛋白相互作用并影响生存信号,突出其作为AKI治疗点的潜力.

关键词:

急性管状亡症的发生.自自是自的过程.细胞生存信号细胞生存信号盖莱克-3的使用方法脏脏脏是什么?宏观自是一种自行为.

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