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Neuroprotective effects of mildronate in a rat model of traumatic brain injury

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dc.contributor.authorYEGEN, BERRAK
dc.contributor.authorsDemir, Dilan; Bektasoglu, Pinar Kuru; Koyuncuoglu, Turkan; Kandemir, Cansu; Akakin, Dilek; Yuksel, Meral; Celikoglu, Erhan; Yegen, Berrak C.; Gurer, Bora
dc.date.accessioned2022-03-12T22:38:36Z
dc.date.available2022-03-12T22:38:36Z
dc.date.issued2019
dc.description.abstractObjective: Traumatic brain injury (TBI) is one of the most common preventable causes of mortality and morbidity. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophysiological mechanisms underlying neuronal loss after TBI. Mildronate is demonstrated to be beneficial in various experimental models of ischemic diseases via anti-inflammatory, antioxidant, and neuroprotective mechanisms. This study aimed to investigate possible antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of mildronate in a rat model of TBI. Methods: A total of 46 male rats were divided into three groups of control, saline-treated TBI, and mildronate-treated TBI. Both TBI groups were subjected to closed-head contusive weight-drop injuries followed by treatment with saline or mildronate (100 mg/kg) administered intraperitoneally. The forebrain was removed 24h after trauma induction, the activities of myeloperoxidase (MPO) and caspase-3, levels of superoxide dismutase (SOD), luminol- and lucigenin-enhanced chemiluminescence were measured, and histomorphological evaluation of cerebral tissues was performed. Results: Increased MPO and caspase-3 activities in the vehicle-treated TBI group (p < 0.001) were suppressed in the mildronate-treated TBI group (p < 0.001). Similarly, increase in luminol and lucigenin levels (p < 0.001 and p < 0.01, respectively) in the vehicle-treated TBI group were decreased in the mildronatetreated TBI group (p < 0.001). Concomitantly, in the vehicle-treated TBI group, TBI-induced decrease in SOD activity (p < 0.01) was reversed with mildronate treatment (p < 0.05). On histopathological examination, TBI-induced damage in the cerebral cortex was lesser in the mildronate-treated TBI group than that in other groups. Conclusion: This study revealed for the first time that mildronate, exhibits neuroprotective effects against TBI because of its anti-inflammatory, antiapoptotic, and antioxidant activities. (C) 2019 Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.injury.2019.08.036
dc.identifier.eissn1879-0267
dc.identifier.issn0020-1383
dc.identifier.pubmed31481152
dc.identifier.urihttps://hdl.handle.net/11424/235680
dc.identifier.wosWOS:000493975800002
dc.language.isoeng
dc.publisherELSEVIER SCI LTD
dc.relation.ispartofINJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAntiapoptotic effect
dc.subjectDiffuse brain injury
dc.subjectMildronate
dc.subjectNeuroprotection
dc.subjectCEREBRAL-BLOOD-FLOW
dc.subjectISCHEMIA-REPERFUSION INJURY
dc.subjectACID OXIDATION INHIBITORS
dc.subjectSPINAL-CORD ISCHEMIA
dc.subjectGAMMA-BUTYROBETAINE
dc.subjectISCHEMIA/REPERFUSION INJURY
dc.subjectCARNITINE BIOSYNTHESIS
dc.subjectSUPEROXIDE-DISMUTASE
dc.subjectPROTEIN EXPRESSION
dc.subjectDARBEPOETIN-ALPHA
dc.titleNeuroprotective effects of mildronate in a rat model of traumatic brain injury
dc.typearticle
dspace.entity.typePublication
local.avesis.id45091e06-3aa5-4308-91b0-a1dae3bbc011
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages7
local.journal.quartileQ2
oaire.citation.endPage1592
oaire.citation.issue10
oaire.citation.startPage1586
oaire.citation.titleINJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED
oaire.citation.volume50
relation.isAuthorOfPublicatione4eaf9ac-f8dc-4e2b-b940-895cc906790d
relation.isAuthorOfPublication.latestForDiscoverye4eaf9ac-f8dc-4e2b-b940-895cc906790d

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