在健康和心脏功能障碍的小鼠模型中,Trastuzumab的心脏毒性和药物心脏保护
Serena L'Abbate1, Matilde Masini2, Giuseppina Nicolini3
1CNR, Institute of Clinical Physiology, Pisa, Italy; Health Science Interdisciplinary Center, Scuola Superiore Sant'Anna, Pisa, Italy.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|August 29, 2025
概括
即使已经存在心脏问题,Trastuzumab (TRZ) 也会引起心脏毒性. 在小鼠模型中,联合卡普托普里尔 (ACEi) 和比索普罗罗尔 (BB) 治疗可以预防TRZ诱导的心脏损伤.
科学领域:
- 心脏病学
- 药理学
- 癌症学
背景情况:
- 预先存在的心血管疾病是HER2向疗法如trastuzumab (TRZ) 的心脏毒性风险因素.
- 关于TRZ对先前存在的心脏病和心脏保护药物的疗效的影响的研究有限.
研究的目的:
- 在不同程度的心脏损伤的小鼠模型中研究TRZ诱导的心脏毒性.
- 在这些模型中评估卡普托普利 (ACEi) 和比索普罗罗尔 (BB) 的心脏保护作用.
主要方法:
- 成年小鼠模型 (健康,心脏高质,心脏功能障碍) 被随机分配到安慰剂,单独使用TRZ或与ACEi/ BB一起使用TRZ.
- 治疗后对心脏功能,心肌组织学,超结构和基因表达进行了评估.
主要成果:
- 在所有组中,TRZ减少了约10%的缩功能,并导致细胞/ 线粒体损伤,不论基线心脏状况如何.
- 在已有心脏功能障碍的小鼠中观察到最严重的副作用.
- 在所有组中,ACEi/ BB联合治疗改善了心脏功能,并逆转了TRZ诱导的细胞和分子损伤.
结论:
- 无论心脏功能如何,TRZ诱导的心脏毒性都会发生.
- 在患有心脏功能障碍和没有心脏功能障碍的模型中,ACEi/ BB联合治疗显示出显著的心脏保护潜力.
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