Evidence map›Paper›PMID 38977337›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024

[Exogenous leptin improves cerebral ischemia-reperfusion-induced glutamate excitotoxic injury in mice by up-regulating GLT-1 and GLAST expression in astrocytes].

J Chen, C Liu, C Wang, L Li, W Tao, J Xun, H Tang, L Huang

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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

J ChenDepartment of Pathophysiology, Bengbu Medical University, Bengbu 233000, China.
C LiuDepartment of Pathophysiology, Bengbu Medical University, Bengbu 233000, China.
C WangPreclinical and Clinical Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Bengbu Medical University, Bengbu 233000, China.
L LiDepartment of Pathophysiology, Bengbu Medical University, Bengbu 233000, China.
W TaoDepartment of Pathophysiology, Bengbu Medical University, Bengbu 233000, China.
J XunSchool of Clinical Medicine, Bengbu Medical University, Bengbu 233000, China.
H TangSchool of Clinical Medicine, Bengbu Medical University, Bengbu 233000, China.
L HuangDepartment of Pathophysiology, Bengbu Medical University, Bengbu 233000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion (I/R) injury in mice and explore the underlying mechanism.

methodsA total of 100 C57BL/6 mice were randomly divided into 5 groups, including a sham-operated group, cerebral I/R model group, and 3 leptin treatment groups with intraperitoneal injections of 0.5, 1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery. At 24 h after reperfusion, neurological function scores of the mice were assessed, and TTC staining was used to determine the area of cerebral infarction. The pathological changes in the cortical brain tissue of the mice were observed using HE staining, and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining. The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting. In another 45 C57BL/6 mice with sham operation, I/R modeling, or leptin (1 mg/kg) treatment, glutamic acid in the cortical brain tissue was detected using glutamate assay, and cortical glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) protein expressions were detected using immunohistochemistry.

resultsCompared with the I/R model mice, the leptin-treated mice had significantly lower neurological deficit scores, smaller cerebral infarct area, milder pathologies in the cortical brain tissue, and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes. Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.

conclusionExogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice, mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.

Indexed as

AstrocytesBrain IschemiaExcitatory Amino Acid Transporter 1Excitatory Amino Acid Transporter 2Glutamic AcidLeptinMice, Inbred C57BLReperfusion InjuryAnimalsDisease Models, AnimalGlial Fibrillary Acidic ProteinMaleMiceNeuronsNeuroprotective AgentsUp-RegulationExcitatory Amino Acid Transporter 1Excitatory Amino Acid Transporter 2Glial Fibrillary Acidic ProteinGlutamic AcidLeptinNeuroprotective AgentsSlc1a2 protein, mouseSlc1a3 protein, mouseastrocytescerebral ischemia-reperfusion injuryexcitotoxicityglutamate-aspartate transporterglutamate transporter-1leptin

Identifiers

PMID38977337
PMCPMC11237293

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