Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-kappa B Signaling Pathway after Brain Injuryopen access
- Authors
- Alam, Sayed Ibrar; Rehman, Shafiq Ur; Kim, Myeong Ok
- Issue Date
- Feb-2019
- Publisher
- MDPI
- Keywords
- brain injury; nicotinamide; neurodegeneration; synaptic dysfunction; neuroinflammation
- Citation
- JOURNAL OF CLINICAL MEDICINE, v.8, no.2
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF CLINICAL MEDICINE
- Volume
- 8
- Number
- 2
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/9486
- DOI
- 10.3390/jcm8020271
- ISSN
- 2077-0383
- Abstract
- Brain injuries are a serious global health issue and are the leading cause of neurodegeneration. To date, there is no proper cure and treatment for brain-injury-induced neuropathological conditions because of a lack of sufficient knowledge and the failure to develop a drug due to the multi-pathological conditions in the brain. Herein, we explored the neurotherapeutic effects of Nicotinamide (NAM), against brain injury-induced neurodegeneration and behavioral problems. Treating injured mouse brains with NAM, for 7 days, significantly ameliorated several pathological events. Interestingly, NAM treatment significantly inhibited the injury-induced activation of receptor for advanced glycation end-products (RAGE), c-Jun N-terminal kinases (JNK), and neuroinflammatory mediators, such as NF-kappa B, TNF-alpha, IL-1 beta, and NOS2 in the brain, and it also regulated the levels of apoptotic markers, including Bax, caspase-3, and Bcl-2. Furthermore, treatment using NAM in TBI mice, significantly reversed synaptic protein loss and improved memory impairments and behavioral outcomes. Our findings suggested that NAM treatment reduced injury-induced secondary neurodegenerative pathology by modulating RAGE/JNK/NF-kappa B signaling in mice. Therefore, we recommend that NAM would be a safe and efficient therapeutic agent against brain-injury-induced neurodegeneration.
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