NAMPT inhibitor protects ischemic neuronal injury in rat brain via anti-neuroinflammation

Neuroscience
Chen-Xiang ChenYun-Bi Lu

Abstract

Nicotinamide phosphoribosyltransferase (NAMPT) is an important neuroprotective factor in cerebral ischemia, and it has been reported that NAMPT inhibitors can aggravate neuronal injury in the acute phase. However, because it is a cytokine, NAMPT participates in many inflammatory diseases in the peripheral system, and its inhibitors have therapeutic effects. Following cerebral ischemia, the peripheral and resident inflammatory and immune cells produce many pro-inflammatory mediators in the ischemic area, which induce neuroinflammation and impair the brain. However, the effects of NAMPT inhibitors in the neuroinflammation after ischemic brain injury remain unknown. Here, we found that FK866, a potent NAMPT inhibitor, decreased the level of TNF-α, NAMPT and IL-6 in the ischemic brain tissue one day after middle-cerebral-artery occlusion and reperfusion (MCAO/R), improved neurological dysfunction, decreased infarct volume and neuronal loss, and inhibited microgliosis and astrogliosis 14days after MCAO/R. The expression of NAMPT protein was induced in Iba1-positive microglia/macrophages in the ischemia core 14days after MCAO/R. In vitro studies show that oxygen-glucose deprivation and recovery (OGD/R) activate microglia. Activated m...Continue Reading

Citations

Apr 18, 2020·Annals of Clinical and Translational Neurology·Zhongju TanWei Gao
Sep 12, 2018·Journal of Molecular Neuroscience : MN·Na LuHaixia Lu
Jan 5, 2020·Acta Physiologica·Roldan M de GuiaJonas T Treebak
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