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氧化物减弱了DOX诱导的培养老鼠肌细胞中的心脏毒性

Celal Guven¹, Eylem Taskin², Özgül Aydın³

¹Department of Biophysics, Faculty of Medicine, Adıyaman University, Adıyaman, Turkey.

Biotechnic & histochemistry : official publication of the Biological Stain Commission

|March 5, 2024

概括

氧化物 (DIA) 通过维护线粒体功能和减少氧化应激来防止多克索鲁比 (DOX) 诱导的心脏毒性. 这项研究表明,DIA可能是预防化疗相关心脏损伤的潜在治疗剂.

科学领域:

心脏病学心脏病学
药理学药理学是指药理学的学科.
细胞生物学细胞生物学

背景情况:

doxorubicin (DOX) 化疗可以引起心脏毒性,导致心肌细胞损失.
线粒体ATP敏感通道 (mitoK_ATP) 与细胞保护有关.
氧化物 (DIA) 是一个已知的mitoK_ATP通道开放剂.

研究的目的:

为了研究氧化物 (DIA) 在培养大鼠心肌细胞中对多克索鲁比 (DOX) 诱导的心脏毒性的保护作用.
探索特定蛋白质和通路 (包括线粒体功能和氧化应激标志物) 在这种保护机制中的作用.

主要方法:

培养的老鼠心肌细胞 (H9c2细胞系) 被单独用DOX治疗或与DOX和DIA联合治疗24小时.
评估的参数包括:乙烯丝分布,线粒体膜潜力,超氧化解突变酶 (SOD) 活性,总氧化剂/抗氧化剂状态 (TOS/TAS),以及蛋白质表达 (ERK1/2,细胞色素c).

主要成果:

DOX治疗降低了SOD活性,增加了ERK1/2水平,并使线粒体膜脱极化.
与DIA联合治疗抵消了这些影响,保持了SOD活性和线粒体潜力.
DIA改善了DOX诱导的细胞骨损伤,降低了ERK1/2和细胞染色体c水平,并增强了mitoK_ATP完整性,特别是在SUR2A升高的情况下.

结论:

氧化物 (DIA) 显示出对多克索鲁比 (DOX) 诱导的心脏毒性的保护作用.
保护机制包括维护mitoK_ATP通道的完整性和调节SOD/AMPK/ERK1/2通路.
DIA是预防化疗引起的心脏损伤的潜在候选者.

关键词:

对ATP敏感的通道细胞灭亡 (apoptosis) 是一种死亡的过程.亚氧化物亚氧化物德克索鲁比辛 (doxorubicin) 是一种药物.氧化应激是一种氧化应激.

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