Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 Oct;39:287-294.
doi: 10.1016/j.intimp.2016.07.036. Epub 2016 Aug 5.

Treatment With NAD(+) Inhibited Experimental Autoimmune Encephalomyelitis by Activating AMPK/SIRT1 Signaling Pathway and Modulating Th1/Th17 Immune Responses in Mice

Affiliations

Treatment With NAD(+) Inhibited Experimental Autoimmune Encephalomyelitis by Activating AMPK/SIRT1 Signaling Pathway and Modulating Th1/Th17 Immune Responses in Mice

Jueqiong Wang et al. Int Immunopharmacol. .

Abstract

Nicotinamide adenine dinucleotide (NAD(+)) plays vital roles in mitochondrial functions, cellular energy metabolism and calcium homeostasis. In this study, we investigated the effect of NAD(+) administration for the treatment of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. EAE, a classical animal model of multiple sclerosis (MS), was induced by subcutaneous injection of myelin oligodendrocyteglycoprotein (MOG). The mice were treated with 250mg/kg (body weight) NAD(+) in PBS administered intraperitoneally once daily. We observed that NAD(+) treatment could lessen the severity of EAE. Additionally, NAD(+) treatment attenuated pathological injuries of EAE mice. We also found that the AMP-activated protein kinase (AMPK)/silent mating-type information regulation 2 homolog 1(SIRT1) pathway was activated in the NAD(+)-treated mice and NAD(+) treatment suppressed pro-inflammatory T cell responses. Our findings demonstrated that NAD(+) could be an effective and promising agent to treat multiple sclerosis and its effects on other autoimmune diseases should be explored.

Keywords: AMPK/SIRT1; Experimental autoimmune encephalomyelitis; Immunomodulatory effect; Multiple sclerosis; NAD(+).

Similar articles

See all similar articles

Cited by 5 articles

Feedback