Research Paper Volume 16, Issue 16 pp 11904—11916

Downregulating miR-432-5p exacerbates adriamycin-induced cardiotoxicity via activating the RTN3 signaling pathway

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Figure 1. Adriamycin (ADR) treatment damages cardiomyocyte and impaired cardiac function of C57BL/6 mice. (A) Cardiomyocytes were treated by a serial of ADR, and ADR decreases the viability of cardiomyocytes; (BD) ADR stimulates oxidative stress and inflammatory response. ADR causes increasing of intracellular reactive oxygen species (ROS) (A) and interleukin-1β (IL-β) (B) lactate dehydrogenase (LDH) (C) level, and LDH levels in primary cardiomyocytes (D); (E) ADR causes obvious decreasing of body weight, and impaired left ventricular ejection fraction (LVEF) and left ventricular systolic function (LVSF) in mice (F); (G) Hematoxylin and Eosin (H&E) staining in ADR-treated myocardium of mice. Increased collagen between muscle, irregular arrangement of myocardial cell nuclei, granular and interstitial hemorrhage could be observed. **p < 0.01, ***p < 0.001.