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烟酰胺腺嘌呤二核苷酸补充剂未能增强啮齿动物的麻醉恢复。

Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents.

作者信息

Goodnough Candida L, Montoya July, Cartusciello Erica B, Floranda Erin L, Gross Eric R

机构信息

Department of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford University, Stanford, USA.

出版信息

Sci Rep. 2025 Jan 9;15(1):1428. doi: 10.1038/s41598-024-83500-6.

DOI:10.1038/s41598-024-83500-6
PMID:39789056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11718248/
Abstract

Nicotinamide Adenine Dinucleotide (NAD) is implicated in bioenergetics, DNA repair, and senescence. Depletion of NAD is associated with aging and neurodegenerative disease, prompting a growing interest in NAD supplementation. With rising over-the-counter use of NAD, understanding their impact on anesthetic recovery becomes essential. This study investigates the effect of NADH, a common NAD precursor, on anesthesia in rodents. Baseline and post-anesthesia (1.5% isoflurane) open field and Y-maze activity were recorded in adult male and female C57BL/6 mice (n = 8-10/group). NADH (150 mg/kg, intraperitoneal) or vehicle (0.9% normal saline) were given at baseline or during anesthesia. The NADH-treated group exhibited a significant decrease in open-field activity relative to vehicle-treated. This diminished activity was reflected in reduced distance travelled and average velocity after emergence from anesthesia in the NADH-treated group. NADH treatment did not improve Y-maze performance after anesthesia, partly related to reduced locomotor activity in the NADH-treated group. This study demonstrates that NADH does not appear to hasten recovery from anesthesia. Instead, there was a depression in open-field activity and no change in Y-maze performance with NADH supplementation, indicators of locomotive and cognitive recovery in rodents. The broad implications of NAD in aging are likely to shape supplementation trends, highlighting the importance of understanding the potential influence of administering NAD on anesthetic sensitivity and recovery.

摘要

烟酰胺腺嘌呤二核苷酸(NAD)与生物能量学、DNA修复和衰老有关。NAD的消耗与衰老和神经退行性疾病相关,这促使人们对补充NAD的兴趣日益增加。随着非处方使用NAD的增加,了解其对麻醉恢复的影响变得至关重要。本研究调查了常见的NAD前体NADH对啮齿动物麻醉的影响。记录成年雄性和雌性C57BL/6小鼠(每组n = 8 - 10只)的基线和麻醉后(1.5%异氟烷)旷场和Y迷宫活动。在基线或麻醉期间给予NADH(150 mg/kg,腹腔注射)或载体(0.9%生理盐水)。与载体处理组相比,NADH处理组的旷场活动显著降低。这种活动减少反映在NADH处理组麻醉苏醒后行进距离和平均速度的降低。NADH处理并未改善麻醉后的Y迷宫表现,部分原因与NADH处理组运动活动减少有关。本研究表明,NADH似乎并未加速麻醉恢复。相反,补充NADH后旷场活动受到抑制,Y迷宫表现没有变化,而旷场活动和Y迷宫表现是啮齿动物运动和认知恢复的指标。NAD在衰老中的广泛影响可能会塑造补充趋势,凸显了解补充NAD对麻醉敏感性和恢复的潜在影响的重要性。

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CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism.CD38通过一种依赖SIRT3的机制决定与年龄相关的NAD下降和线粒体功能障碍。
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