Ginsenoside Re protects against kainate-induced neurotoxicity in mice by attenuating mitochondrial dysfunction through activation of the signal transducers and activators of transcription 3 signaling
DC Field | Value | Language |
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dc.contributor.author | Nguyen, YenNhiDoan | - |
dc.contributor.author | Jeong, JiHoon | - |
dc.contributor.author | Sharma, Naveen | - |
dc.contributor.author | Tran, Ngoc KimCuong | - |
dc.contributor.author | Tran, Hoang-Yen Phi | - |
dc.contributor.author | Dang, Duy-Khanh | - |
dc.contributor.author | Park, JungHoon | - |
dc.contributor.author | Byun, Jae Kyung | - |
dc.contributor.author | Ko, Sung Kwon | - |
dc.contributor.author | Nah, Seung-Yeol | - |
dc.contributor.author | Kim, Hyoung-Chun | - |
dc.contributor.author | Shin, Eun-Joo | - |
dc.date.accessioned | 2024-04-29T07:30:53Z | - |
dc.date.available | 2024-04-29T07:30:53Z | - |
dc.date.issued | 2024-04 | - |
dc.identifier.issn | 1071-5762 | - |
dc.identifier.issn | 1029-2470 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/73495 | - |
dc.description.abstract | It was demonstrated that ginsenosides exert anti-convulsive potentials and interleukin-6 (IL-6) is protective from excitotoxicity induced by kainate (KA), a model of temporal lobe epilepsy. Ginsenosides-mediated mitochondrial recovery is essential for attenuating KA-induced neurotoxicity, however, little is known about the effects of ginsenoside Re (GRe), one of the major ginsenosides. In this study, GRe significantly attenuated KA-induced seizures in mice. KA-induced redox changes were more evident in mitochondrial fraction than in cytosolic fraction in the hippocampus of mice. GRe significantly attenuated KA-induced mitochondrial oxidative stress (i.e., increases in reactive oxygen species, 4-hydroxynonenal, and protein carbonyl) and mitochondrial dysfunction (i.e., the increase in intra-mitochondrial Ca2+ and the decrease in mitochondrial membrane potential). GRe or mitochondrial protectant cyclosporin A restored phospho-signal transducers and activators of transcription 3 (STAT3) and IL-6 levels reduced by KA, and the effects of GRe were reversed by the JAK2 inhibitor AG490 and the mitochondrial toxin 3-nitropropionic acid (3-NP). Thus, we used IL-6 knockout (KO) mice to investigate whether the interaction between STAT3 and IL-6 is involved in the GRe effects. Importantly, KA-induced reduction of manganese superoxide dismutase (SOD-2) levels and neurodegeneration (i.e., astroglial inhibition, microglial activation, and neuronal loss) were more prominent in IL-6 KO than in wild-type (WT) mice. These KA-induced detrimental effects were attenuated by GRe in WT and, unexpectedly, IL-6 KO mice, which were counteracted by AG490 and 3-NP. Our results suggest that GRe attenuates KA-induced neurodegeneration via modulating mitochondrial oxidative burden, mitochondrial dysfunction, and STAT3 signaling in mice. | - |
dc.format.extent | 17 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | TAYLOR & FRANCIS LTD | - |
dc.title | Ginsenoside Re protects against kainate-induced neurotoxicity in mice by attenuating mitochondrial dysfunction through activation of the signal transducers and activators of transcription 3 signaling | - |
dc.type | Article | - |
dc.identifier.doi | 10.1080/10715762.2024.2341885 | - |
dc.identifier.bibliographicCitation | Free radical research, v.58, no.4, pp 276 - 292 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 001206990200001 | - |
dc.identifier.scopusid | 2-s2.0-85191194754 | - |
dc.citation.endPage | 292 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 276 | - |
dc.citation.title | Free radical research | - |
dc.citation.volume | 58 | - |
dc.type.docType | Article | - |
dc.publisher.location | 영국 | - |
dc.subject.keywordAuthor | Hippocampus | - |
dc.subject.keywordAuthor | IL-6 knockout mice | - |
dc.subject.keywordAuthor | Kainate seizures | - |
dc.subject.keywordAuthor | Mitochondrial dysfunction | - |
dc.subject.keywordAuthor | Oxidative stress | - |
dc.subject.keywordAuthor | STAT3 signaling | - |
dc.subject.keywordPlus | TRIMETHYLTIN-INDUCED NEUROTOXICITY | - |
dc.subject.keywordPlus | CU/ZN-SUPEROXIDE-DISMUTASE | - |
dc.subject.keywordPlus | KINASE-C-DELTA | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | NEURONAL VULNERABILITY | - |
dc.subject.keywordPlus | INTERLEUKIN-6 PROTECTS | - |
dc.subject.keywordPlus | HIPPOCAMPAL-NEURONS | - |
dc.subject.keywordPlus | ANTIEPILEPTIC DRUGS | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | CULTURES | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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