DSpace at EWHA약학대학약학과Journal papers
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dc.contributor.author서은경*
dc.date.accessioned2025-08-07T07:10:39Z-
dc.date.available2025-08-07T07:10:39Z-
dc.date.issued2025*
dc.identifier.issn0009-2797*
dc.identifier.otherOAK-37385*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/271944-
dc.description.abstractTraumatic brain injury (TBI) is an acquired neurological insult that has become a major cause of mortality.Hence, immediate and appropriate medical attention is essential. The present study investigated the neuroprotective effect of 7β-(3-ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z-notonipetranone (ECN), a sesquiterpenoid against a weight drop model of traumatic brain injury (TBI). During the in-vitro analysis, ECN demonstrated neuroprotective potential by remarkably improving the cell viability and also provided significant protection in case of nitric oxide-evoked oxidative stress in HT22 cells. The administration of ECN significantly improved the neurological severity score, and mechanical/periorbital allodynia following TBI, when compared with the TBI-group. The level of brain edema and blood-brain barrier (BBB) disruption were also significantly reduced by ECN treatment. ECN also restored constitutional changes in the protein/lipid profile; simultaneous with histological changes in the brain in contrast to the TBI-group. It significantly ameliorated neuronal loss and also minimized the intracerebral hemorrhages arising from traumatic insult. ECN exhibited potent anti-inflammatory effects, by altering the expression of extracellular-signal-regulated kinase (ERK), p38, and activating protein-1 (AP-1) proteins. It also exhibited antioxidant effects by increasing the production levels of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Furthermore, ECN also produced an anti-apoptotic effect by downregulation of caspase3 and upregulation of B-cell lymphoma 2 (Bcl-2). It also increased the levels of antioxidants while reducing the levels of oxidative stress and inflammatory markers in comparison to the TBI-group. In short, it was concluded that ECN exhibited protective anti-inflammatory, antioxidant, and anti-apoptotic effects against trauma-induced brain injury. © 2025 Elsevier B.V., All rights reserved.*
dc.languageEnglish*
dc.publisherElsevier Ireland Ltd*
dc.subjectAntioxidants*
dc.subjectApoptosis*
dc.subjectEcn*
dc.subjectInflammation*
dc.subjectNeuroprotection*
dc.subjectTraumatic Brain Injury*
dc.subjectCaspase 3*
dc.subjectCatalase*
dc.subjectCrystal Violet*
dc.subjectEosin*
dc.subjectGlutathione*
dc.subjectGlutathione Transferase*
dc.subjectHematoxylin*
dc.subjectMitogen Activated Protein Kinase*
dc.subjectMyeloperoxidase*
dc.subjectNitric Oxide*
dc.subjectProtein Bcl 2*
dc.subjectSuperoxide Dismutase*
dc.subjectHeme Oxygenase-1*
dc.subjectMitogen-activated Protein Kinases*
dc.subjectNeuroprotective Agents*
dc.subjectNf-e2-related Factor 2*
dc.subjectNfe2l2 Protein, Mouse*
dc.subjectSesquiterpenes*
dc.subjectGraph Pad Version 8.0.1.244*
dc.subjectImage J Software*
dc.subjectOrigin Pro Software V 9.6.5.169*
dc.subjectSkanit Re 4.1*
dc.subject7beta (3 Ethyl Cis Crotonoyloxy) 1alpha (2 Methylbutyryloxy) 3,14 Dehydro Z Notonipetranone*
dc.subjectAntioxidant*
dc.subjectHeme Oxygenase 1*
dc.subjectInterleukin 1beta*
dc.subjectLipid Peroxidase*
dc.subjectReactive Oxygen Metabolite*
dc.subjectSesquiterpenoid*
dc.subjectSynaptophysin*
dc.subjectTranscription Factor Ap 1*
dc.subjectTranscription Factor Nrf2*
dc.subjectTumor Necrosis Factor*
dc.subjectUnclassified Drug*
dc.subjectNeuroprotective Agent*
dc.subjectSesquiterpene*
dc.subjectAnimal Cell*
dc.subjectAnimal Experiment*
dc.subjectAnimal Model*
dc.subjectAnimal Tissue*
dc.subjectAntiinflammatory Activity*
dc.subjectAntioxidant Activity*
dc.subjectArticle*
dc.subjectBlood Brain Barrier*
dc.subjectBrain Edema*
dc.subjectBrain Hemorrhage*
dc.subjectCell Viability*
dc.subjectDifferential Scanning Calorimetry*
dc.subjectFourier Transform Infrared Spectroscopy*
dc.subjectHistology*
dc.subjectHt22 Cell Line*
dc.subjectImmunohistochemistry*
dc.subjectIn Vitro Study*
dc.subjectMale*
dc.subjectMapk Signaling*
dc.subjectMechanical Allodynia*
dc.subjectMouse*
dc.subjectMtt Assay*
dc.subjectNeurologic Disease Assessment*
dc.subjectNeurological Severity Scoring*
dc.subjectNonhuman*
dc.subjectNrf2 Ho 1 Signaling*
dc.subjectOxidative Stress*
dc.subjectReal Time Polymerase Chain Reaction*
dc.subjectScoring System*
dc.subjectSignal Transduction*
dc.subjectThermogravimetry*
dc.subjectVon Frey Test*
dc.subjectAnimal*
dc.subjectCell Line*
dc.subjectCell Survival*
dc.subjectChemistry*
dc.subjectDrug Effect*
dc.subjectDrug Therapy*
dc.subjectMetabolism*
dc.subjectPathology*
dc.subjectAnimals*
dc.subjectBlood-brain Barrier*
dc.subjectBrain Injuries, Traumatic*
dc.subjectMice*
dc.title7β-(3-ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z-notonipetranone (ECN) attenuates inflammation and oxidative stress via MAPK, and Nrf2/HO-1 signaling in Traumatic brain injury*
dc.typeArticle*
dc.relation.volume415*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.journaltitleChemico-Biological Interactions*
dc.identifier.doi10.1016/j.cbi.2025.111510*
dc.identifier.wosidWOS:001473799600001*
dc.identifier.scopusid2-s2.0-105002579508*
dc.author.googleZafar S.*
dc.author.googleJamil M.*
dc.author.googleKhan M.I.*
dc.author.googleDin F.U.*
dc.author.googleSeo E.K.*
dc.author.googleKhan S.*
dc.contributor.scopusid서은경(7005953758)*
dc.date.modifydate20261006123658*
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