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烟酰胺单核苷酸（NMN）在视网膜脱离光感受器退行性变模型中的神经保护作用及其作用机制。

Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment.

机构信息

Angiogenesis Laboratory, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA 02114, USA.

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China.

出版信息

Aging (Albany NY). 2020 Dec 29;12(24):24504-24521. doi: 10.18632/aging.202453.

DOI:10.18632/aging.202453
PMID:33373320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7803565/
Abstract

Currently, no pharmacotherapy has been proven effective in treating photoreceptor degeneration in patients. Discovering readily available and safe neuroprotectants is therefore highly sought after. Here, we investigated nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD), in a retinal detachment (RD) induced photoreceptor degeneration. NMN administration after RD resulted in a significant reduction of TUNEL photoreceptors, CD11b macrophages, and GFAP labeled glial activation; a normalization of protein carbonyl content (PCC), and a preservation of the outer nuclear layer (ONL) thickness. NMN administration significantly increased NAD levels, SIRT1 protein expression, and heme oxygenase-1 (HO-1) expression. Delayed NMN administration still exerted protective effects after RD. Mechanistic studies using 661W cells revealed a SIRT1/HO-1 signaling as a downstream effector of NMN-mediated protection under oxidative stress and LPS stimulation. In conclusion, NMN administration exerts neuroprotective effects on photoreceptors after RD and oxidative injury, suggesting a therapeutic avenue to treating photoreceptor degeneration.

摘要

目前，尚无药物疗法被证明能有效治疗患者的光感受器变性。因此，人们非常希望能发现易于获得且安全的神经保护剂。在这里，我们研究了烟酰胺单核苷酸（NMN），烟酰胺腺嘌呤二核苷酸（NAD）的前体，在视网膜脱离（RD）诱导的光感受器变性中的作用。RD 后给予 NMN 治疗可显著减少 TUNEL 阳性光感受器、CD11b 巨噬细胞和 GFAP 标记的神经胶质细胞激活；可使蛋白羰基含量（PCC）正常化，并维持外核层（ONL）厚度。NMN 治疗可显著增加 NAD 水平、SIRT1 蛋白表达和血红素加氧酶-1（HO-1）表达。RD 后延迟给予 NMN 仍能发挥保护作用。使用 661W 细胞进行的机制研究表明，在氧化应激和 LPS 刺激下，NMN 介导的保护作用的下游效应物为 SIRT1/HO-1 信号。总之，NMN 治疗可在 RD 和氧化损伤后对光感受器发挥神经保护作用，为治疗光感受器变性提供了一种治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a02f/7803565/72d986ed0415/aging-12-202453-g007.jpg
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