ArticleMolecular biology reports2022
Combination of nicotinamide mononucleotide and troxerutin induces full protection against doxorubicin-induced cardiotoxicity by modulating mitochondrial biogenesis and inflammatory response.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- An integrated anti-aging framework targeting NADRedox biology · 2026Review
- Nicotinamide mononucleotide induces lipolysis by regulating ATGL expression via the SIRT1-AMPK axis in adipocytes.Biochemistry and biophysics reports · 2023Article
- Rodent Models of Dilated Cardiomyopathy and Heart Failure for Translational Investigations and Therapeutic Discovery.International journal of molecular sciences · 2023Review
- Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundClinical application of doxorubicin (DOX) is restricted due to its cardiotoxicity, reinforcing the significance of exploring new strategies to counteract DOX-induced cardiotoxicity. The present work aimed to investigate the ameliorative impact of combination therapy with nicotinamide mononucleotide (NMN) and troxerutin (TXR) on DOX-induced cardiotoxicity, with mitochondrial function/biogenesis and inflammatory response approach.
methodsMale Wistar rats (n = 30, 250-300 g) were divided into groups with/without DOX and/or NMN and TXR, alone or in combination. Rats underwent 6 consecutive intraperitoneal injections of DOX (cumulative dose: 12 mg/kg). NMN (100 mg/kg/day; intraperitoneally) and/or TXR (150 mg/kg/day; orally) were administered for 28 days before DOX challenge. Seven days following the last injection of DOX, evaluation of cardiac histopathological changes, BNP and LDH levels, mitochondrial function (membrane potential, ROS generation, and ATP levels), expression of proteins involved in mitochondrial biogenesis (PGC-1α, NRF1, and TFAM), and inflammatory cytokines (TNF-α, IL-1β, and IL-6) was performed.
resultsCombination of NMN and TXR significantly decreased the severity of histopathological damages, and BNP and LDH levels (P < 0.01 to P < 0.001). It also restored mitochondrial functional endpoints, and expression of proteins involved in mitochondrial biogenesis (P < 0.05 to P < 0.001), and decreased inflammatory cytokines (P < 0.01 to P < 0.001). The positive impacts of this combination therapy were more potent as compared to monotherapies.
conclusionsThese findings shed new light on the understanding of additive properties of NMN/TXR combination therapy in protecting against DOX-induced cardiotoxicity. The cardioprotective effect of this combination therapy may be mediated in part through the restoration of mitochondrial function/biogenesis associated with the PGC-1α/NRF1/TFAM pathway, and suppression of inflammatory response.
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