Delayed administration of the GLP-1 receptor agonist liraglutide improves metabolic and functional recovery after cerebral ischemia in rats
| Autor: | Fahuan Song, Aiying Chen, Min Cheng, Gaoli Zheng, Wenbin Dong, Yunping Miao, Xiaodi Ye |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Agonist Male medicine.medical_specialty medicine.drug_class Ischemia Nerve Tissue Proteins Neuroprotection Glucagon-Like Peptide-1 Receptor Brain Ischemia 03 medical and health sciences Eating 0302 clinical medicine Adenosine Triphosphate Internal medicine medicine Animals Neuropeptide Y Stroke Mice Knockout biology Glial fibrillary acidic protein Cerebral infarction Liraglutide business.industry General Neuroscience Membrane Proteins medicine.disease Mice Inbred C57BL 030104 developmental biology Endocrinology nervous system biology.protein NeuN business Energy Metabolism 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neuroscience letters. 641 |
| ISSN: | 1872-7972 |
| Popis: | Glucagon-like peptide 1 receptor (GLP-1R) agonists administered before or immediately after induction of experimental stroke have been shown to provide acute neuroprotection. Here, we determined whether delayed treatment with a GLP-1R agonist could improve metabolic and functional recovery after stroke. Rats were subjected to middle cerebral artery occlusion (MCAO) and given the well-established GLP-1R agonist liraglutide (50, 100, or 200μg/kg) or normal saline (NS) daily for 4 weeks, starting 1 day after MCAO. Cerebral glucose metabolism and neurological deficits were evaluated using 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) imaging and modified neurological severity score (mNSS) test. Levels of neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), von Willebrand factor (vWF), and GLP-1R were assessed by immunohistochemical staining and Western blot analysis. PET imaging showed that animals treated with liraglutide had significantly higher 18F-FDG accumulation in the cerebral infarction compared with animals treated with NS. Liraglutide significantly reduced the mNSS score. It also greatly increased the expression of NeuN, GFAP, vWF, and GLP-1R in the cerebral ischemic area at postoperative week 4. These results demonstrated metabolic and functional recovery after delayed treatment with liraglutide in a rat model of cerebral ischemia. |
| Databáze: | OpenAIRE |
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