期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 77, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2019.105918
关键词
1-Methylnicotinamide; Lipopolysaccharide; Cognition deficits; Neuroinflammation; Neuronal apoptosis
资金
- National Natural Science Foundation of China [81573413, 81773714, 81273497, 81603113]
- Double First-Class University Project [CPU2018GF/GY**]
- Fundamental Research Funds for the Central Universities [2632017PT01]
Alzheimer's disease (AD) is a neurodegenerative disease that affects cognition and behavior. The neuroinflammatory response in the brain is an important pathological characteristic in AD. In this study, we investigated the neuroprotective effects of 1-Methylnicotinamide (MNA), known as the main metabolite of nicotinamide, on reducing lipopolysaccharide (LPS)-induced cognitive deficits via targeting neuroinflammation and neuronal apoptosis. We found that the mice treated with LPS exhibited cognitive deficits in the novel object recognition, Morris water maze and Y-maze avoidance tests. However, intragastric administration of MNA (100 or 200 mg/kg) for 3 weeks significantly attenuated LPS-induced cognitive deficits in mice. Importantly, MNA treatment suppressed the protein expression of nuclear factor-kappa B p65 (NF-kappa B p65), pro-inflammatory cytokines (TNF-alpha, IL-6) and decreased the activation of microglia and astrocytes in the hippocampus and frontal cortex of LPS-induced mice. In addition, MNA treatment suppressed neuronal apoptosis by reducing the number of TUNEL-positive cells, caspase-3 activation and increasing the level of Bcl-2/Bax ratio in the hippocampus and frontal cortex. These findings indicate that MNA could be a potential neuroprotective drug in neurodegenerative diseases such as AD.
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