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尼古丁胺胺单核酸补充剂可以缓解多克索鲁比诱导的多器官纤维化

Fei Wen¹, Anhua Xu¹, Wenjing Wei¹

¹Key Laboratory of Regenerative Medicine of Ministry of Education, Institute of Aging and Regenerative Medicine, Department of Developmental & Regenerative Medicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.

International journal of molecular sciences

|May 25, 2024

概括

尼古丁胺胺单核酸 (NMN) 抗击了多克索鲁比 (DOX) 的毒性. 补充NMN可以减少化学疗法引起的多器官损伤和死亡率,恢复尼古丁胺氨酸二核酸 (NAD+) 水平.

科学领域:

生物医学科学生物医学科学
药理学药理学是指药理学的学科.
毒理学毒理学毒理学

背景情况:

doxorubicin (DOX) 是一种重要的化疗药物,具有显著的多器官毒性,特别是心脏毒性,限制了其使用.
由DOX引起的毒性,包括DNA损伤和氧化应激,与尼古丁胺氨酸二核酸 (NAD+) 水平降低有关.

研究的目的:

评估尼古丁胺胺 mononucleotide (NMN) 的疗效,一个NAD+前体,在缓解多克索鲁比 (DOX) 诱导的多器官毒性.
调查NMN抵消DOX相关不良影响的潜在机制.

主要方法:

研究人员使用了一种小鼠模型,给出了多克索鲁比辛 (DOX) 来诱导多器官毒性.
尼古丁胺胺单核酸 (NMN) 被用于评估其对DOX诱导损伤的保护作用.
在DOX治疗和NMN治疗小鼠中测量了NAD+水平,组织纤维化,巨细胞透和死亡率.

主要成果:

多克索鲁比 (DOX) 的使用显著降低了心脏,肝脏和肺部等重要器官的NAD+水平.
尼古丁胺胺单核酸 (NMN) 治疗减轻了多器官纤维化和减少了小鼠的死亡率.
补充NMN缓解了DOX诱导的组织纤维化,巨细胞透和细胞损伤,与NAD+恢复相关.

结论:

尼古丁胺胺单核酸 (NMN) 有效地抵消与多克索鲁比 (DOX) 化疗相关的多器官毒性.
通过NMN补充恢复NAD+是一种有前途的策略,可以减轻化疗引起的器官损伤并改善患者的治疗结果.

关键词:

它们是NAD+NAD+NAD.德克索鲁比辛 (doxorubicin) 是一种药物.纤维化纤维化多器官损伤多器官损伤尼古丁胺胺 mononucleotide 的使用情况

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