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阿斯坦丁通过调节PTP1B/JNK通路在体外抑制LPS诱导的心肌亡

Wen-Jie Xie¹, Miao Liu², Xu Zhang³

¹Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.

International immunopharmacology

|December 23, 2023

概括

阿斯塔克桑丁 (ATX) 通过抑制亡,防止败血症引起的心肌损伤. ATX 向蛋白氨酸酸酶1B (PTP1B) 并抑制 JNK 信号通路,减少细胞死亡.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
败血症研究败血症研究

背景情况:

败血症引起的心肌损伤是死亡的一个重要原因.
心肌亡在感染性心肌损伤的发病过程中起着至关重要的作用.
阿斯塔克桑丁 (ATX) 正在研究其潜在的心脏保护作用.

研究的目的:

在体外探索阿斯塔ξαν丁 (ATX) 抑制脂多糖 (LPS) 诱导的心肌亡的机制.
确定ATX对抗败血性心肌损伤的保护作用所涉及的分子标和信号通路.

主要方法:

用LPS和不同度的ATX,PTP1B抑制剂或JNK激活剂对待H9C2细胞.
评估了细胞活力 (CCK-8测定),细胞亡 (流细胞计) 和线粒体膜潜力 (JC-1染色).
预测了ATX的分子标 (SwissTargetPrediction) 并验证了 (MST);分析了PTP1B,JNK和p-JNK的蛋白质表达 (西方斑点,免疫光).

主要成果:

ATX增强了H9C2细胞活力,并抑制了LPS诱导的亡和线粒体功能障碍.
蛋白氨酸酸酶1B (PTP1B) 被确定为ATX的直接目标.
ATX减弱了LPS诱导的PTP1B和p-JNK表达,并通过PTP1B/JNK通路抑制了亡.

结论:

阿斯塔克桑丁 (ATX) 有效地抑制H9C2细胞中脂聚糖 (LPS) 诱导的线粒体亡.
保护机制涉及PTP1B/JNK信号通路,PTP1B被确定为ATX的直接分子标.
ATX显示了缓解与败血症相关的心肌损伤的显著潜力.

关键词:

阿斯塔克桑丁是一种阿斯塔克桑丁.在JNK信号传输中.脂聚糖类糖化物脂聚糖类糖化物线粒体的亡是线粒体的亡.蛋白质氨酸酸酶1B是一种蛋白质氨酸酸酶1B.

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