Alpha-Linolenic Acid Impedes Cadmium-Induced Oxidative Stress, Neuroinflammation, and Neurodegeneration in Mouse Brain
DC Field | Value | Language |
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dc.contributor.author | Alam, Sayed-Ibrar | - |
dc.contributor.author | Kim, Min-Woo | - |
dc.contributor.author | Shah, Fawad Ali | - |
dc.contributor.author | Saeed, Kamran | - |
dc.contributor.author | Ullah, Rahat | - |
dc.contributor.author | Kim, Myeong-Ok | - |
dc.date.accessioned | 2022-12-26T10:01:05Z | - |
dc.date.available | 2022-12-26T10:01:05Z | - |
dc.date.created | 2022-12-12 | - |
dc.date.issued | 2021-09 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gnu/handle/sw.gnu/3311 | - |
dc.description.abstract | Alpha-Linolenic acid (ALA), an omega-3 polyunsaturated fatty acid, is extracted from plant sources and has been shown to be one of the anti-inflammatory and antioxidant agents. Herein, we revealed the molecular mechanism underlying the anti-inflammatory and antioxidant potential of (ALA), against cadmium in the adult mouse brain. We evaluated the neuroprotective effect of ALA (60 mg/kg per oral for 6 weeks) against CdCl2 (5 mg/kg)-induced oxidative stress, neuroinflammation, and neuronal apoptosis. According to our findings, ALA markedly reduced ROS production and nitric oxide synthase 2 (NOS2) and enhanced the expression of nuclear factor-2 erythroid-2 (Nrf-2) and heme oxygenase-1 (HO-1) in mice treated with CdCl2. Most importantly, the molecular docking study revealed that ALA allosterically decreases the overexpression of c-Jun N-terminal kinase (JNK) activity and inhibited the detrimental effect against CdCl2. Moreover, ALA suppressed CdCl2-induced glial fibrillary acidic protein (GFAP), nuclear factor-kappa b (NF-kappa B), and interleukin-1 beta (IL-1 beta) in the mouse brain. Further, we also checked the pro- and anti-apoptotic proteins markers such as Bax, Bcl-2, and caspase-3, which were regulated in the cortex of ALA co-treated mouse brain. Overall, our study suggests that oral administration of ALA can impede oxidative stress, neuroinflammation, and increase neuronal apoptosis in the cortex of Cd-injected mouse brain. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | LIPID-PEROXIDATION | - |
dc.subject | APOPTOSIS | - |
dc.subject | ENZYME | - |
dc.subject | DAMAGE | - |
dc.subject | MODEL | - |
dc.title | Alpha-Linolenic Acid Impedes Cadmium-Induced Oxidative Stress, Neuroinflammation, and Neurodegeneration in Mouse Brain | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Myeong-Ok | - |
dc.identifier.doi | 10.3390/cells10092274 | - |
dc.identifier.scopusid | 2-s2.0-85115887663 | - |
dc.identifier.wosid | 000699113700001 | - |
dc.identifier.bibliographicCitation | CELLS, v.10, no.9 | - |
dc.relation.isPartOf | CELLS | - |
dc.citation.title | CELLS | - |
dc.citation.volume | 10 | - |
dc.citation.number | 9 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | LIPID-PEROXIDATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | ENZYME | - |
dc.subject.keywordPlus | DAMAGE | - |
dc.subject.keywordPlus | MODEL | - |
dc.subject.keywordAuthor | cadmium | - |
dc.subject.keywordAuthor | reactive oxygen species (ROS) | - |
dc.subject.keywordAuthor | Nrf2 | - |
dc.subject.keywordAuthor | HO-1 | - |
dc.subject.keywordAuthor | neuroinflammation | - |
dc.subject.keywordAuthor | neurodegeneration | - |
dc.subject.keywordAuthor | p-JNK | - |
dc.subject.keywordAuthor | Alpha Linolenic acid | - |
dc.subject.keywordAuthor | neuroprotection | - |
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