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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
鲁丁减轻了皮拉鲁比辛引起的心脏毒性,并增强了乳腺癌中的化学敏感性
1Huzhou Central Hospital, Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, No. 1558 Sanhuan North Road, Huzhou, 313000 Zhejiang Province, China; Huzhou Central Hospital, Affiliated Central Hospital of Huzhou University, No. 1558 Sanhuan North Road, Huzhou, 313000 Zhejiang Province, China; Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, 1266 Fujin Road, Changchun, Jilin 130021, China.
鲁丁通过调节miR-129-1-3p/GRIN2D通路来保护皮拉鲁比辛的心脏毒性,并增强其在乳腺癌中的抗癌作用. 这一发现为更安全,更有效的化疗提供了一个新的治疗点.
科学领域:
- 生物医学科学 生物医学科学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 乳腺癌的Pirarubicin (THP) 化疗受剂量依赖性心脏毒性限制.
- 素是一种黄类化合物,对心脏保护和抗癌活性有希望,但其机制尚不清楚.
研究的目的:
- 研究miR-129-1-3p/GRIN2D轴在鲁丁的心脏保护和化学敏感作用中的作用.
- 阐明基于THP的化疗中,路丁的双重益处背后的分子机制.
主要方法:
- 使用了一种双重疾病的小鼠模型 (4T1乳腺瘤).
- 接受THP与或没有鲁丁或miR-129-1-3p的小鼠.
- 评估了心脏功能,氧化应激,心肌酶,平衡和瘤进展.
主要成果:
- 通过减少氧化应激,心肌细胞亡和恢复平衡,素减轻了THP诱导的心脏毒性.
- 鲁丁增强了THP的抗瘤功效,抑制了瘤生长和转移,同时增加了亡.
- 常规调节了miR-129-1-3p,它准并抑制了GRIN2D,减少了氧化应激和心脏和瘤组织中的过量.
结论:
- 鲁抗击THP心脏毒性,并通过miR-129-1-3p/GRIN2D通路改善化疗.
- miR-129-1-3p是这个轴的关键中间体.
- 鲁丁-miR-129-1-3p-GRIN2D途径为提高乳腺癌化疗安全性和疗效提供了一个有希望的目标.
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