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乙胆受体激动剂有效地减弱了多重程序细胞死亡途径,并在老鼠中改善左心室功能
Nanthip Prathumsap1, Benjamin Ongnok1, Thawatchai Khuanjing1
1Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand.
Life sciences
|July 23, 2023
概括
乙胆受体 (AChR) 的激活可以通过防止心肌细胞死亡来保护免受特拉斯图祖马布 (TRZ) 诱导的心脏毒性. 这表明,ACHR激动剂可能是未来的治疗方法,以减轻癌症患者的TRZ心脏毒性.
科学领域:
- 在瘤学瘤学.
- 心脏病学 心脏病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 对于癌症而言,trastuzumab (TRZ) 治疗可能会导致衰弱的心脏毒性,可能导致不可逆转的心脏功能障碍和心肌细胞死亡.
- 已知乙胆受体 (AChR) 激活可以预防各种心脏病,但其在缓解TRZ诱导心脏毒性 (TIC) 中的作用仍然未被探索.
研究的目的:
- 研究乙胆受体 (AChR) 激动剂对特拉斯图祖马布 (TRZ) 诱导的心脏毒性 (TIC) 的潜在心脏保护作用.
- 探索ICT的潜在机制以及ACHR激活如何影响这些过程.
主要方法:
- 四十只成年雄性Wistar大鼠被随机分为五组:对照组,单独使用TRZ,TRZ加上α7nAChR激活剂 (PNU-282987),TRZ加上mAChR激活剂 (贝坦霍尔),TRZ加上组合治疗.
- 使用H9c2细胞进行了体外研究,以验证ACHR激活的细胞保护作用.
主要成果:
- 由TRZ诱导的心脏毒性表现为线粒体功能障碍,自功能受损以及通过热,铁和亡的显著肌细胞死亡.
- 单独和组合的α7nAChR和mAChR激动剂显著缓解了这些病理变化,并保护了心脏功能.
- AChR激活在体外显示出细胞保护作用,但不影响TRZ的抗癌性质,亡并没有涉及TIC的发展.
结论:
- 激活α7nAChR和mAChR通路可以有效地减轻TRZ诱导的心脏毒性.
- AChR激动剂代表了一种有前途的治疗策略,用于预防或治疗与TRZ疗法相关的心脏毒性.
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