Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway.

ABSTRACT: Replenishment of NAD⁺ has been shown to protect against brain disorders such as amyotrophic lateral sclerosis and ischemic stroke. However, whether this intervention has therapeutic effects in intracerebral hemorrhage (ICH) is unknown. In this study, we sought to determine the potential therapeutic value of replenishment of NAD⁺ in ICH. In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD⁺) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD⁺. NMN treatment did not decrease hematoma volume and hemoglobin content. However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammati

SUBMITTER: Wei CC 

PROVIDER: S-EPMC5429727 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature