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首页> 外文期刊>CNS neuroscience & therapeutics. >Extracellular Visfatin has Nicotinamide Phosphoribosyltransferase Enzymatic Activity and is Neuroprotective Against Ischemic Injury
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Extracellular Visfatin has Nicotinamide Phosphoribosyltransferase Enzymatic Activity and is Neuroprotective Against Ischemic Injury

机译：细胞外Visfatin具有烟酰胺磷酸核糖基转移酶的酶活性，对缺血性损伤具有神经保护作用

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Summary Aim Visfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and exists in intracellular and extracellular compartments. The intracellular form of visfatin is proved to be nicotinamide phosphoribosyltransferase ( NAMPT ) and exhibits neuroprotection through maintaining intracellular NAD + pool. However, whether extracellular form of visfatin has NAMPT activity and the effect of extracellular visfatin in cerebral ischemia are unknown. Methods and Results Plasma concentrations of visfatin, NAD +, and ATP were increased in mice upon cerebral ischemia. Cultured glia, but not neuron, was able to secrete visfatin. Oxygen‐glucose deprivation ( OGD ) stress increased the secretion of visfatin from glia. Extracellular recombinant mouse wild‐type visfatin, but not mouse H247A‐mutant enzymatic‐dead visfatin, had NAMPT enzymatic function in vitro . Treatment of wild‐type visfatin, but not H247A‐mutant enzymatic‐dead visfatin, significantly attenuated detrimental effect of OGD on the cell viability and apoptosis in both cultured mouse neuron and glia. Treatment of neutralizing antibody, abolished the protective effect of extracellular visfatin on cell viability, but failed to block the antiapoptotic effect of extracellular visfatin. At last, we observed that plasma visfatin concentrations decreased in 6‐month‐old but not 3‐month‐old SHR ‐ SP compared with that in age‐matched Wistar‐Kyoto rats. Inhibition of NAMPT enzymatic function of visfatin (by FK 866) accelerated the occurrence of stroke in SHR ‐ SP . Conclusions Extracellular visfatin has NAMPT enzymatic activity and maybe be neuroprotective just as intracellular visfatin in cerebral ischemic injury.
机译：总结Aim Visfatin是一种新型的脂肪因子，主要由内脏脂肪组织产生，并存在于细胞内和细胞外区室。 visfatin的细胞内形式被证明是烟酰胺磷酸核糖基转移酶（NAMPT），并且通过维持细胞内NAD +池而表现出神经保护作用。但是，尚不清楚胞外形式的visfatin是否具有NAMPT活性以及胞外visfatin在脑缺血中的作用尚不清楚。方法和结果脑缺血后，小鼠血浆中的visfatin，NAD +和ATP浓度升高。培养的神经胶质细胞，但不是神经元，能够分泌visfatin。缺氧缺氧（OGD）压力增加了胶质细胞中visfatin的分泌。细胞外重组小鼠野生型visfatin在体外具有NAMPT酶的功能，但没有小鼠H247A突变型酶促死的visfatin。野生型visfatin的治疗可显着减弱OGD对培养的小鼠神经元和神经胶质细胞活力和细胞凋亡的有害作用，但不能抑制H247A突变的酶促死亡visfatin。中和抗体的处理，取消了细胞外visfatin对细胞活力的保护作用，但未能阻止细胞外visfatin的抗凋亡作用。最后，我们观察到，与年龄匹配的Wistar-Kyoto大鼠相比，在6个月大但3个月大的SHR-SP中血浆visfatin浓度降低了。抑制visfatin的NAMPT酶功能（通过FK 866）加速了SHR-SP中风的发生。结论细胞外visfatin具有NAMPT酶活性，可能与脑内visfatin在脑缺血性损伤中一样具有神经保护作用。

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