伊内泰塔马布通过与亡,氧化应激和自途径的相互作用引发心脏毒性
Weiqun Wang1,2, Hongliang Zhang3, Yikun Qu3
1The Basic Medical College, Jiamusi University, Jiamusi, 154007, Heilongjiang, China.
Scientific reports
|July 2, 2025
概括
伊内泰塔马布是特拉斯图祖马布的生物类似物,它通过促进细胞死亡和氧化应激引起心脏损伤. 这项研究揭示了Inetetamab心肌细胞和体内模型中心脏毒性背后的机制.
科学领域:
- 心脏病学 心脏病学
- 在瘤学瘤学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 伊内泰塔马布是一种被批准用于治疗HER2阳性转移性乳腺癌的trastuzumab生物类似药.
- 已经认识到伊内泰坦的心脏毒性潜力,但其潜在的机制需要阐明.
研究的目的:
- 为了研究因内泰他马布诱导的心脏毒性的机制.
- 在体外和体外评估伊内泰塔马布对心肌细胞的影响.
主要方法:
- 在体外研究中,使用暴露于Inetetamab的H9c2心肌细胞.
- 在体内研究中,使用了用Inetetamab.治疗的小鼠模型.
- 评估细胞活力,细胞亡,自,线粒体膜潜力,ROS产量和氧化应激标志物 (MDA,GSH/GSSG).
- 在体内测量心脏损伤生物标志物 (CK-MB,BNP,cTnI).
主要成果:
- 暴露于inetetamab降低了H9c2细胞活力,改变了细胞形态.
- 伊内泰塔马布诱导了亡,自,减少了线粒体膜潜力,并在H9c2细胞中增加了ROS.
- 在体内,Inetetamab导致心肌细胞损伤,心脏生物标志物升高,并诱导了亡和氧化应激.
- 在体外和体内观察到与亡和自相关的蛋白质的调节.
结论:
- 伊内泰他马布通过涉及亡,氧化应激和自的机制诱导心脏毒性.
- 这些发现为Inetetamab的心脏毒性作用提供了洞察力,这对于用这种生物类似药治疗的患者的管理至关重要.
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