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烟酰胺通过 NAD+-依赖性去乙酰化机制预防糖尿病性脑炎症。

Nicotinamide Prevents Diabetic Brain Inflammation via NAD+-Dependent Deacetylation Mechanisms.

机构信息

Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), 08041 Barcelona, Spain.

Departamento de Bioquímica y Biología Molecular B e Inmunología, Facultad de Medicina, Universidad de Murcia (UMU), 30120 Murcia, Spain.

出版信息

Nutrients. 2023 Jul 9;15(14):3083. doi: 10.3390/nu15143083.

DOI:10.3390/nu15143083
PMID:37513501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10383777/
Abstract

This study investigated the effect of nicotinamide (NAM) supplementation on the development of brain inflammation and microglial activation in a mouse model of type 1 diabetes mellitus. C57BL/6J male mice, which were made diabetic with five consecutive, low-dose (55 mg/kg i.p.) streptozotocin (STZ) injections. Diabetic mice were randomly distributed in different experimental groups and challenged to different doses of NAM (untreated, NAM low-dose, LD, 0.1%; NAM high-dose, HD, 0.25%) for 25 days. A control, non-diabetic group of mice was used as a reference. The NAD+ content was increased in the brains of NAM-treated mice compared with untreated diabetic mice (NAM LD: 3-fold; NAM HD: 3-fold, -value < 0.05). Immunohistochemical staining revealed that markers of inflammation (TNFα: NAM LD: -35%; NAM HD: -46%; -value < 0.05) and microglial activation (IBA-1: NAM LD: -29%; NAM HD: -50%; -value < 0.05; BDKRB1: NAM LD: -36%; NAM HD: -37%; -value < 0.05) in brains from NAM-treated diabetic mice were significantly decreased compared with non-treated T1D mice. This finding was accompanied by a concomitant alleviation of nuclear NFκB (p65) signaling in treated diabetic mice (NFκB (p65): NAM LD: -38%; NAM HD: -53%, -value < 0.05). Notably, the acetylated form of the nuclear NFκB (p65) was significantly decreased in the brains of NAM-treated, diabetic mice (NAM LD: -48%; NAM HD: -63%, -value < 0.05) and inversely correlated with NAD+ content (r = -0.50, -value = 0.03), suggesting increased activity of NAD+-dependent deacetylases in the brains of treated mice. Thus, dietary NAM supplementation in diabetic T1D mice prevented brain inflammation via NAD+-dependent deacetylation mechanisms, suggesting an increased action of sirtuin signaling.

摘要

这项研究旨在探讨烟酰胺（NAM）补充对 1 型糖尿病小鼠模型中脑炎症和小胶质细胞激活发展的影响。C57BL/6J 雄性小鼠连续 5 次接受低剂量（55mg/kg ip）链脲佐菌素（STZ）注射，制成糖尿病模型。糖尿病小鼠被随机分配到不同的实验组，并接受不同剂量的 NAM（未处理、NAM 低剂量、LD、0.1%；NAM 高剂量、HD、0.25%）处理 25 天。一组非糖尿病对照小鼠作为参考。与未经处理的糖尿病小鼠相比，接受 NAM 治疗的小鼠脑中 NAD+含量增加（NAM LD：增加 3 倍；NAM HD：增加 3 倍，p 值 < 0.05）。免疫组织化学染色显示，炎症标志物（TNFα：NAM LD：减少 35%；NAM HD：减少 46%，p 值 < 0.05）和小胶质细胞激活标志物（IBA-1：NAM LD：减少 29%；NAM HD：减少 50%，p 值 < 0.05；BDKRB1：NAM LD：减少 36%；NAM HD：减少 37%，p 值 < 0.05）在 NAM 治疗的糖尿病小鼠脑中明显减少。这一发现伴随着 NFκB（p65）核信号的同时减轻（NFκB（p65）：NAM LD：减少 38%；NAM HD：减少 53%，p 值 < 0.05）。值得注意的是，在接受 NAM 治疗的糖尿病小鼠脑中，NFκB（p65）的乙酰化形式显著减少（NAM LD：减少 48%；NAM HD：减少 63%，p 值 < 0.05），并与 NAD+含量呈负相关（r = -0.50，p 值 = 0.03），提示 NAD+依赖性去乙酰化酶在治疗小鼠脑中的活性增加。因此，糖尿病 T1D 小鼠的饮食 NAM 补充通过 NAD+依赖性去乙酰化机制预防脑炎症，提示 Sirtuin 信号的作用增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d1/10383777/208813fe5d9e/nutrients-15-03083-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d1/10383777/43d52ec8cac4/nutrients-15-03083-g001.jpg
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