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Effects of co-administration of metformin and evogliptin on cerebral infarct volume in the diabetic rat

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dc.contributor.authorLee, SJ-
dc.contributor.authorYoon, BS-
dc.contributor.authorHong, JM-
dc.contributor.authorJoe, EH-
dc.contributor.authorLee, JS-
dc.date.accessioned2023-02-27T07:12:45Z-
dc.date.available2023-02-27T07:12:45Z-
dc.date.issued2022-
dc.identifier.issn0014-4886-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/24858-
dc.description.abstractPatients with diabetes suffer more severe ischemic stroke. A combination of metformin and dipeptidyl peptide-4 inhibitors is commonly prescribed to treat diabetes. Therefore, we aimed to determine if pretreatment with a combination of metformin and evogliptin, a dipeptidyl peptidase-4 inhibitor, could reduce cerebral infarct volume in rats with streptozotocin-induced diabetes. After confirming diabetes induction, the rats were treated with vehicle, evogliptin, metformin, or evogliptin/metformin combination for 30 days. Then, stroke was induced by transient middle cerebral artery occlusion (tMCAO). Infarct volume, oxidative stress, levels of methylglyoxal-modified protein, glucagon-like peptide-1 receptor (GLP-1R), AMPK, and Akt/PI3K pathway-related proteins, and post-stroke pancreatic islet cell volume were evaluated. Compared to vehicle, only the co-administration group had significantly reduced infarct volume from the effects of tMCAO; the regimen also improved glycemic control, whereas the individual treatments did not. Co-administration also significantly reduced methylglyoxal-modified protein level in the core of the brain cortex, and the expression of 4-HNE and 8-OHdG was reduced. Co-administration increased p-Akt levels in the ischemic core and mitigated the suppression of Bcl-2 expression. Plasma GLP-1 and dipeptidyl peptidase-4 levels and brain GLP-1R expression remained unaltered. In the pancreas, islet cell damage was reduced by co-administration. These results reveal that metformin and evogliptin co-administration ameliorates cerebral infarction associated with prolonged glycemic control and pancreatic beta cell sparing. Other potential protective mechanisms may be upregulation of insulin receptor signaling or reduction of methylglyoxal-induced neurotoxicity. The combination of metformin and evogliptin should be tested further for its potential against focal cerebral ischemia in diabetes patients.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHBrain Chemistry-
dc.subject.MESHCerebral Infarction-
dc.subject.MESHCerebrovascular Circulation-
dc.subject.MESHDiabetes Mellitus, Experimental-
dc.subject.MESHDrug Therapy, Combination-
dc.subject.MESHHypoglycemic Agents-
dc.subject.MESHInfarction, Middle Cerebral Artery-
dc.subject.MESHInsulin-Secreting Cells-
dc.subject.MESHMagnetic Resonance Imaging-
dc.subject.MESHMale-
dc.subject.MESHMetformin-
dc.subject.MESHOxidative Stress-
dc.subject.MESHPiperazines-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReperfusion Injury-
dc.subject.MESHSignal Transduction-
dc.subject.MESHStroke-
dc.titleEffects of co-administration of metformin and evogliptin on cerebral infarct volume in the diabetic rat-
dc.typeArticle-
dc.identifier.pmid34780772-
dc.subject.keywordDiabetes mellitus-
dc.subject.keywordEvogliptin-
dc.subject.keywordIschemic stroke-
dc.subject.keywordMetformin-
dc.subject.keywordNeuroprotection-
dc.contributor.affiliatedAuthorLee, SJ-
dc.contributor.affiliatedAuthorHong, JM-
dc.contributor.affiliatedAuthorJoe, EH-
dc.contributor.affiliatedAuthorLee, JS-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.expneurol.2021.113922-
dc.citation.titleExperimental neurology-
dc.citation.volume348-
dc.citation.date2022-
dc.citation.startPage113922-
dc.citation.endPage113922-
dc.identifier.bibliographicCitationExperimental neurology, 348. : 113922-113922, 2022-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.identifier.eissn1090-2430-
dc.relation.journalidJ000144886-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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