Melatonin ameliorates microvessel abnormalities in the cerebral cortex and hippocampus in a rat model of Alzheimer's disease.

Melatonin ameliorates microvessel abnormalities in the cerebral cortex and hippocampus in a rat model of Alzheimer's disease.
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外源性血小板衍生生长因子改善脊髓损伤后神经血管单元的恢复

DOI:
10.4103/1673-5374.295349
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发表时间:
2021-04
影响因子:
6.1
通讯作者:
Lai H
Lai H
中科院分区:
医学2区
文献类型:
--
作者:
Wang P;Sui HJ;Li XJ;Bai LN;Bi J;Lai H

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褪黑激素能减轻心脏微血管缺血/再灌注损伤,但褪黑激素是否也能改善脑微血管异常尚不清楚。通过六次脑室内注射淀粉样蛋白β 1-42建立阿尔茨海默病大鼠模型,每隔一天给药一次。连续13天腹膜内施用褪黑激素(30 mg/kg),其中第一剂量在第一次施用淀粉样蛋白β 1-42之前24小时给予。褪黑素可改善Morris水迷宫实验中的学习记忆障碍,改善大脑皮层和海马微血管形态,增加微血管密度,减轻脑神经元病理损伤,降低血管内皮生长因子及其受体1和2的表达。这些研究结果表明,褪黑素可以通过降低血管内皮生长因子及其受体的表达,改善大脑皮层和海马区的微血管异常,从而改善阿尔茨海默病患者的认知功能。本研究于2018年12月6日获得中国锦州医科大学动物管理与使用委员会批准(批准号:2019015)。
Melatonin can attenuate cardiac microvascular ischemia/reperfusion injury, but it remains unclear whether melatonin can also ameliorate cerebral microvascular abnormalities. Rat models of Alzheimer’s disease were established by six intracerebroventricular injections of amyloid-beta 1–42, administered once every other day. Melatonin (30 mg/kg) was intraperitoneally administered for 13 successive days, with the first dose given 24 hours prior to the first administration of amyloid-beta 1–42. Melatonin ameliorated learning and memory impairments in the Morris water maze test, improved the morphology of microvessels in the cerebral cortex and hippocampus, increased microvessel density, alleviated pathological injuries of cerebral neurons, and decreased the expression of vascular endothelial growth factor and vascular endothelial growth factor receptors 1 and 2. These findings suggest that melatonin can improve microvessel abnormalities in the cerebral cortex and hippocampus by lowering the expression of vascular endothelial growth factor and its receptors, thereby improving the cognitive function of patients with Alzheimer’s disease. This study was approved by the Animal Care and Use Committee of Jinzhou Medical University, China (approval No. 2019015) on December 6, 2018.
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