Melatonin attenuates D-galactose-induced memory impairment, neuroinflammation and neurodegeneration via RAGE/NF-B-K/JNK signaling pathway in aging mouse model
DC Field | Value | Language |
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dc.contributor.author | Ali, Tahir | - |
dc.contributor.author | Badshah, Haroon | - |
dc.contributor.author | Kim, Tae Hyun | - |
dc.contributor.author | Kim, Myeong Ok | - |
dc.date.accessioned | 2022-12-26T21:51:11Z | - |
dc.date.available | 2022-12-26T21:51:11Z | - |
dc.date.created | 2022-12-13 | - |
dc.date.issued | 2015-01 | - |
dc.identifier.issn | 0742-3098 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gnu/handle/sw.gnu/17513 | - |
dc.description.abstract | Melatonin acts as a pleiotropic agent in various age-related neurodegenerative diseases. In this study, we examined the underlying neuroprotective mechanism of melatonin against D-galactose-induced memory and synaptic dysfunction, elevated reactive oxygen species (ROS), neuroinflammation and neurodegeneration. D-galactose was administered (100mg/kg intraperitoneally (i.p.)) for 60days. After 30days of D-galactose administration, vehicle (same volume) or melatonin (10mg/kg, i.p.) was administered for 30days. Our behavioral (Morris water maze and Y-maze test) results revealed that chronic melatonin treatment alleviated D-galactose-induced memory impairment. Additionally, melatonin treatment reversed D-galactose-induced synaptic disorder via increasing the level of memory-related pre-and postsynaptic protein markers. We also determined that melatonin enhances memory function in the D-galactose-treated mice possibly via reduction of elevated ROS and receptor for advanced glycation end products (RAGE). Furthermore, Western blot and morphological results showed that melatonin treatment significantly reduced D-galactose-induced neuroinflammation through inhibition of microgliosis (Iba-1) and astrocytosis (GFAP), and downregulating other inflammatory mediators such as p-IKK, p-NF-(K)B65, COX2, NOS2, IL-1, and TNF. Moreover, melatonin lowered the oxidative stress kinase p-JNK which suppressed various apoptotic markers, that is, cytochrome C, caspase-9, caspase-3 and PARP-1, and prevent neurodegeneration. Hence, melatonin attenuated the D-galactose-induced memory impairment, neuroinflammation and neurodegeneration possibly through RAGE/NF-B-K/JNK pathway. Taken together, our data suggest that melatonin could be a promising, safe and endogenous compatible antioxidant candidate for age-related neurodegenerative diseases such as Alzheimer's disease (AD). | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | AMELIORATES COGNITION DEFICITS | - |
dc.subject | NF-KAPPA-B | - |
dc.subject | ALZHEIMERS-DISEASE | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | ACTIVATION | - |
dc.subject | BRAIN | - |
dc.subject | RECEPTOR | - |
dc.subject | DAMAGE | - |
dc.subject | NEUROGENESIS | - |
dc.subject | INVOLVEMENT | - |
dc.title | Melatonin attenuates D-galactose-induced memory impairment, neuroinflammation and neurodegeneration via RAGE/NF-B-K/JNK signaling pathway in aging mouse model | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Myeong Ok | - |
dc.identifier.doi | 10.1111/jpi.12194 | - |
dc.identifier.scopusid | 2-s2.0-84919644246 | - |
dc.identifier.wosid | 000346478800007 | - |
dc.identifier.bibliographicCitation | JOURNAL OF PINEAL RESEARCH, v.58, no.1, pp.71 - 85 | - |
dc.relation.isPartOf | JOURNAL OF PINEAL RESEARCH | - |
dc.citation.title | JOURNAL OF PINEAL RESEARCH | - |
dc.citation.volume | 58 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 71 | - |
dc.citation.endPage | 85 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.subject.keywordPlus | AMELIORATES COGNITION DEFICITS | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | BRAIN | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | DAMAGE | - |
dc.subject.keywordPlus | NEUROGENESIS | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordAuthor | D-galactose | - |
dc.subject.keywordAuthor | melatonin | - |
dc.subject.keywordAuthor | memory impairment | - |
dc.subject.keywordAuthor | neurodegeneration | - |
dc.subject.keywordAuthor | neuroinflammation | - |
dc.subject.keywordAuthor | reactive oxygen species | - |
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