Prostaglandin E1 Alleviates Cognitive Dysfunction in Chronic Cerebral Hypoperfusion Rats by Improving Hemodynamics
| Autor: | Li'an Huang, Yu Liao, Weibiao Lu, Chi Kwan Tsang, Xiaomei Xie, Wenxian Li, Yuanfang Chen, Jianye Liang, Zhen Jing |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
endocrine system cognitive functions Angiogenesis cerebral blood flow Hemodynamics Morris water navigation task Vasodilation Pharmacology lcsh:RC321-571 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine.artery medicine neuronal damage Common carotid artery Prostaglandin E1 chronic cerebral hypoperfusion lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research prostaglandin E1 business.industry General Neuroscience 030104 developmental biology medicine.anatomical_structure chemistry Cerebral blood flow lipids (amino acids peptides and proteins) business 030217 neurology & neurosurgery Neuroscience Astrocyte circulatory and respiratory physiology |
| Zdroj: | Frontiers in Neuroscience, Vol 13 (2019) Frontiers in Neuroscience |
| DOI: | 10.3389/fnins.2019.00549/full |
| Popis: | Compensatory vascular mechanisms can restore cerebral blood flow (CBF) but fail to protect against chronic cerebral hypoperfusion (CCH)-mediated neuronal damage and cognitive impairment. Prostaglandin E1 (PGE1) is known as a vasodilator to protect against ischemic injury in animal models, but its protective role in CCH remains unclear. To determine the effect of PGE1 on cerebral hemodynamics and cognitive functions in CCH, bilateral common carotid artery occlusion (BCCAO) was used to mimic CCH in rats, which were subsequently intravenously injected with PGE1 daily for 2 weeks. Magnetic resonance imaging, immunofluorescence staining and Morris water maze (MWM) were used to evaluate CBF, angiogenesis, and cognitive functions, respectively. We found that PGE1 treatment significantly restored CBF by enhancing vertebral artery dilation. In addition, PGE1 treatment increased the number of microvascular endothelial cells and neuronal cells in the hippocampus, and decreased the numbers of astrocyte and apoptotic cells. In the MWM test, we further showed that the escape latency of CCH rats was significantly reduced after PGE1 treatment. Our results suggest that PGE1 ameliorates cognitive dysfunction in CCH rats by enhancing CBF recovery, sustaining angiogenesis, and reducing astrocyte activation and neuronal loss. |
| Databáze: | OpenAIRE |
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