Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) – upregulation of expression; β-secretase 1 (BACE1) – promotion of ubiquitination and proteasomal degradation; Nicotinamide adenine dinucleotide (NAD+) – precursor leading to increased steady-state levels. [2]

烟酰胺核苷（0.5 nM；24 小时）可降低 SOD2 和 Ndufa9 的乙酰化状态 [1]。在 C2C12、Hepa1.6 和 HEK293 细胞中，烟酰胺核苷在 1-1000 μM 的浓度范围内以浓度依赖性方式增加细胞内和线粒体 NAD+ 含量 [1]。烟酰胺核苷支持针对冠状病毒 (CoV)（COVID-19 的病因之一）的先天免疫力，并改善 NAD 和抗病毒聚（ADP-核糖）聚合酶 (PARP) 功能 [3]。

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在源自Tg2576小鼠胚胎的原代皮层-海马神经元培养物中，Nicotinamide riboside 处理显著增加了PGC-1α蛋白水平（通过Western blot分析确定）。这种增加被腺病毒PGC-1α shRNA基因沉默所消除。[2]
在相同的原代神经元培养物中，Nicotinamide riboside 处理降低了BACE1蛋白水平。这种降低在很大程度上被腺病毒PGC-1α shRNA介导的PGC-1α沉默所消除，表明对BACE1的作用是通过PGC-1α介导的。[2]
在稳定转染Myc标签BACE1 (Myc-BACE1)的HEK293细胞中，用Nicotinamide riboside 处理或通过腺病毒感染过表达PGC-1α，增加了泛素化BACE1蛋白的水平（通过免疫沉淀后使用抗泛素抗体进行Western blot检测）。这表明NR促进了BACE1的泛素化。同时，在NR处理或过表达PGC-1α的细胞中，单泛素水平降低。[2]

长期服用烟酰胺核苷（口服；400 mg/kg/天；持续 16 周）会以组织特异性方式提高细胞内和血浆 NAD+ 含量 [1]。

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在7-8月龄的Tg2576阿尔茨海默病模型小鼠中，通过饮用水饮食补充250 mg/kg/天的Nicotinamide riboside 持续3个月，显著改善了在新物体识别测试中的认知表现。处理组小鼠探索新物体的时间为63.2 ± 1.7%，而未处理的对照组为42.0 ± 9.2%。[2]
相同的处理方案（250 mg/kg/天 NR，持续3个月）显著增加了Tg2576小鼠大脑皮层中NAD+的稳态水平。[2]
定量RT-PCR分析表明，与未处理的对照组相比，此NR处理显著增加了Tg2576小鼠脑中PGC-1α的mRNA水平。[2]
酶联免疫吸附测定显示，与安慰剂处理的对照组相比，NR处理的Tg2576小鼠脑中Aβ1-42的水平显著降低。[2]
在来自Tg2576小鼠的海马切片中，应用20 μM Nicotinamide riboside 4小时，消除了在CA1区记录到的长时程增强缺陷。在NR处理的切片中，强直刺激后120分钟的LTP反应为基线水平的224 ± 15%，而对照切片为164 ± 12%。NR灌流不影响野生型小鼠切片的基础突触传递或LTP。[2]
对NR处理3个月的Tg2576小鼠大脑皮层提取物进行定量RT-PCR分析，显示多种线粒体能量代谢相关基因的mRNA水平显著上调，包括柠檬酸合酶、顺乌头酸酶、丙酮酸脱氢酶激酶3、细胞色素c亚基VIc、磷酸甘油酸激酶1和葡萄糖磷酸异构酶1。[2]

蛋白质印迹分析[1]
细胞类型： HEK293T 细胞
测试浓度： 0.5 nM
孵育时间： 24 hrs (hrs (小时))
实验结果：Ndufa9 和 SOD2 的乙酰化状态降低。

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原代皮层-海马神经元培养物从14.5天龄的Tg2576小鼠胚胎脑中制备。解离的细胞接种并在添加了特定生长因子的神经基础培养基中培养。体外培养7天后，细胞用于处理。[2]
对于Western blot分析，用补充了蛋白酶抑制剂的裂解液裂解细胞或脑组织。蛋白裂解物通过SDS-PAGE分离，转印至硝酸纤维素膜，并用针对靶蛋白（如PGC-1α、BACE1、泛素）的一抗孵育，然后使用HRP偶联的二抗和增强化学发光法检测。[2]
对于定量RT-PCR，使用商业试剂盒从组织或细胞中提取总RNA。使用逆转录预混液合成cDNA。使用SYBR Green预混液在实时PCR系统上进行定量PCR，以测量靶基因的mRNA水平。[2]
对于BACE1泛素化实验，用NR处理稳定表达Myc-BACE1的HEK293细胞和/或用腺病毒载体感染。使用抗BACE1抗体对细胞裂解物进行免疫沉淀，然后使用抗泛素抗体对沉淀的蛋白进行Western blot分析，以检测泛素化的BACE1。[2]

Animal/Disease Models: 10weeks old C57Bl/6J mice [1]
Doses: 400 mg/kg
Route of Administration: oral; daily; continued for 16 weeks
Experimental Results: Plasma and intracellular NAD+ levels increased in a tissue-specific manner.

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Seven- to 8-month-old Tg2576 transgenic mice were treated with Nicotinamide riboside at a dose of 250 mg/kg/day, administered via drinking water. The treatment started when mice were 5-6 months old and continued for 3 months until they were 10-11 months old. Control Tg2576 mice received saline in their drinking water. [2]
After the treatment period, cognitive function was assessed using the novel object recognition test. Mice were first habituated to an apparatus and allowed to explore a familiar object. After a delay, they were reintroduced to the apparatus containing the familiar object and a novel object. The time spent exploring each object was recorded. [2]
After behavioral testing, mice were sacrificed. One brain hemisphere was snap-frozen for biochemical analyses (e.g., NAD+ assay, ELISA, Western blot, qRT-PCR), and the other hemisphere was fixed for histopathological examination. [2]
For electrophysiology studies, hippocampal slices (400 μm thick) were prepared from Tg2576 or wild-type mice. Slices were maintained in an interface chamber with artificial cerebrospinal fluid. After recovery, slices were perfused with 20 μM Nicotinamide riboside for 4 hours. Basal synaptic transmission and long-term potentiation were recorded in the CA1 region following standard protocols. [2]

The study demonstrated that dietary administration of Nicotinamide riboside (250 mg/kg/day for 3 months) significantly increased the steady-state levels of NAD+ in the cerebral cortex of Tg2576 mice. [2]

[1]. The NAD(+) precursor nicotinamide riboside enhances oxidative metabolism and protectsagainst high-fat diet-induced obesity. Cell Metab. 2012 Jun 6;15(6):838-47.

[2]. Nicotinamide Riboside Restores Cognition Through an Upregulation of Proliferator-Activated Receptor-γ Coactivator 1α Regulated β-Secretase 1 Degradation and Mitochondrial Gene Expression in Alzheimer's Mouse Models. Neurobiol Aging. 2013 Jun;34(6):1581-8.

[3]. Coronavirus and PARP Expression Dysregulate the NAD Metabolome: A Potentially Actionable Component of Innate Immunity. bioRxiv. 2020 Apr 30;2020.04.17.047480.

N-ribosylnicotinamide is a pyridine nucleoside consisting of nicotinamide with a beta-D-ribofuranosyl moiety at the 1-position. It has a role as a human metabolite, a Saccharomyces cerevisiae metabolite, a mouse metabolite and a geroprotector. It is a N-glycosylnicotinamide and a pyridine nucleoside.
Nicotinamide riboside is under investigation in clinical trial NCT03432871 (Nicotinamide Riboside and Mitochondrial Biogenesis).
Nicotinamide riboside is a metabolite found in or produced by Escherichia coli (strain K12, MG1655).
Nicotinamide riboside has been reported in Drosophila melanogaster, Homo sapiens, and other organisms with data available.
Nicotinamide Riboside is an orally available form of vitamin B3 and precursor of nicotinamide adenine dinucleotide (NAD+) with potential use in the treatment of chemotherapy induced peripheral neuropathy (CIPN). Upon oral administration, nicotinamide riboside (NR) is converted to nicotinamide mononucleotide by the NR kinases, nicotinamide riboside kinase 1 (NRK 1) and nicotinamide riboside kinase 2 (NRK 2), to which a second adenine is transferred by nicotinamide mononucleotide adenylyl transferase to generate NAD+. NAD+, an essential redox coenzyme, may offer protective effects against axonal injury from both mechanical and neurotoxic injury, and maintenance of NAD+ may be protective in mitochondrial disease. NR may help elevate and maintain NAD+ levels, which may ameliorate potential mechanisms implicated in the development of CIPN including mitochondrial dysfunction and peripheral nerve degeneration.
Nicotinamide riboside is a metabolite found in or produced by Saccharomyces cerevisiae.

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Nicotinamide riboside is a precursor of nicotinamide adenine dinucleotide (NAD+). [2]
In the context of Alzheimer's disease models, Nicotinamide riboside is proposed to exert protective effects by upregulating PGC-1α expression. Elevated PGC-1α promotes the ubiquitination and subsequent proteasomal degradation of BACE1, a key enzyme in amyloid-β peptide production. This leads to reduced Aβ levels in the brain. [2]
Additionally, Nicotinamide riboside treatment upregulates the expression of a set of mitochondrial energy metabolism-related genes, which may contribute to improved cognitive function and synaptic plasticity. [2]
The study suggests that Nicotinamide riboside may represent a potential therapeutic strategy for Alzheimer's disease by targeting PGC-1α-mediated pathways to reduce amyloid pathology and improve brain energy metabolism. [2]

C₁₁H₁₅N₂O₅

255.25

255.097

1341-23-7

Nicotinamide riboside chloride;23111-00-4;Nicotinamide riboside tartrate;2415657-86-0;Nicotinamide riboside malate;2415659-01-5

439924

Typically exists as solid at room temperature

1.201g/cm3

353.7ºC at 760mmHg

181.9ºC

3.05E-07mmHg at 25°C

1.549

-2.3

116.25

4

5

3

18

314

4

C1=CC(=C[N+](=C1)[C@H]2[C@@H]([C@@H]([C@H](O2)CO)O)O)C(=O)N

JLEBZPBDRKPWTD-TURQNECASA-O

InChI=1S/C11H14N2O5/c12-10(17)6-2-1-3-13(4-6)11-9(16)8(15)7(5-14)18-11/h1-4,7-9,11,14-16H,5H2,(H-,12,17)/p+1/t7-,8-,9-,11-/m1/s1

1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyridin-1-ium-3-carboxamide

N-RibosylnicotinamideNicotinamide-beta-riboside Nicotinamide ribonucleoside

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
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