Effect of nicotinamide mononucleotide on doxorubicin-induced cardiac injury in mice

Doxorubicin (DOX) is the cornerstone of chemotherapy regimens for many malignancies, but its clinical usage is limited by severe cardiotoxicity. Accumulating evidence suggest that nicotinamide adenine dinucleotide (NAD+) depletion contributes to DOX-induced cardiotoxicity, making NAD+ boosting an appealing strategy. Nicotinamide mononucleotide (NMN) is an NAD+ precursor that shows promising therapeutic effects in various diseases. To understand the impact of NMN on gene expression in myocardial tissue of DOX-exposed mice, a RNA-seq assay was carried out. Overall design: Male C57BL/6 mice aged 8 weeks were treated with a single dose of DOX (15 mg/kg, i.p., Pfizer). Sham mice received the same volume of sterile saline. NMN (500 mg/kg, i.p., ApexBio) or saline was given 30 min prior to DOX injection. After 5 days of DOX administration, mice were sacrificed with hearts harvested and subjected to RNA-seq analysis