Nicotinamide Mononucleotide Administration Prevents Doxorubicin-Induced Cardiotoxicity and Loss in Physical Activity in Mice.
Marielle MargierChisaka KuehnemannNicolas HuloJazmin MoralesPrasanna Vadhana Ashok KumaarCecile CrosHelene CannelleJulie CharmetantEric VerdinMatthias CanaultAlessia GrozioPublished in: Cells (2022)
Doxorubicin (Doxo) is a widely used antineoplastic drug with limited clinical application due to its deleterious dose-related side effects. We investigated whether nicotinamide mononucleotide (NMN) could protect against Doxo-induced cardiotoxicity and physical dysfunction in vivo. To assess the short- and long-term toxicity, two Doxo regimens were tested, acute and chronic. In the acute study, C57BL6/J (B6) mice were injected intraperitoneally (i.p.) once with Doxo (20 mg/kg) and NMN (180 mg/kg/day, i.p.) was administered daily for five days before and after the Doxo injection. In the chronic study, B6 mice received a cumulative dose of 20 mg/kg Doxo administered in fractionated doses for five days. NMN (500 mg/kg/day) was supplied in the mice's drinking water beginning five days before the first injection of Doxo and continuing for 60 days after. We found that NMN significantly increased tissue levels of NAD+ and its metabolites and improved survival and bodyweight loss in both experimental models. In addition, NMN protected against Doxo-induced cardiotoxicity and loss of physical function in acute and chronic studies, respectively. In the heart, NMN prevented Doxo-induced transcriptomic changes related to mitochondrial function, apoptosis, oxidative stress, inflammation and p53, and promyelocytic leukemia nuclear body pathways. Overall, our results suggest that NMN could prevent Doxo-induced toxicity in heart and skeletal muscle.
Keyphrases
- oxidative stress
- drug induced
- diabetic rats
- high glucose
- physical activity
- drinking water
- skeletal muscle
- liver failure
- heart failure
- bone marrow
- body mass index
- metabolic syndrome
- cell proliferation
- emergency department
- insulin resistance
- acute myeloid leukemia
- endothelial cells
- adipose tissue
- ischemia reperfusion injury
- cancer therapy
- high fat diet induced
- mass spectrometry
- cell death
- signaling pathway
- mouse model
- mental health
- aortic dissection
- cell cycle arrest
- rna seq
- stress induced
- acute respiratory distress syndrome
- health risk assessment
- medical education