通过烟碱型乙酰胆碱受体在脑缺血再灌注损伤大鼠中具有抗炎和神经发生功能。
has anti-inflammation and neurogenesis functions through nicotinic acetylcholine receptors in cerebral ischemia-reperfusion injury rats.
作者信息
Ko Cheng-Hang, Huang Chun-Ping, Lin Yi-Wen, Hsieh Ching-Liang
机构信息
Department of Chinese Medicine, China Medical University Hospital, Taichung 40447, Taiwan.
Chinese Medicine Research Center, China Medical University, Taichung 40402, Taiwan.
出版信息
Iran J Basic Med Sci. 2018 Nov;21(11):1174-1178. doi: 10.22038/IJBMS.2018.30371.7322.
OBJECTIVES
(PF) has anti-oxidation, anti-inflammation, anti-apoptosis, and neuroprotection pharmacological effects against ischemic injury. The aim of the present study was to investigate the neuroprotection mechanisms of PF in cerebral ischemia-reperfusion injury rats.
MATERIALS AND METHODS
We established an animal model of cerebral infarct by occlusion of the middle cerebral artery for 15 min, followed by reperfusion, and PF was administered 24 hr later (20 mg/kg, intraperitoneally for 6 days) after reperfusion.
RESULTS
Treatment with PF reduced the neurological deficit score, improved motor function, decreased cell counts of nicotinic acetylcholine receptor (nAChR) α4β2 immunoreactive cells, and increased cell counts of nAChR α7. Furthermore, PF administration suppressed neuronal apoptosis and promoted neurogenesis.
CONCLUSION
PF rescued neurological deficit and underlying mechanisms were inhibition of neurological apoptosis and inflammation by nAChRs.
目的
（PF）对缺血性损伤具有抗氧化、抗炎、抗凋亡和神经保护药理作用。本研究旨在探讨PF对脑缺血再灌注损伤大鼠的神经保护机制。
材料与方法
通过阻断大脑中动脉15分钟，然后再灌注，建立脑梗死动物模型，再灌注24小时后（20毫克/千克，腹腔注射6天）给予PF。
结果
PF治疗降低了神经功能缺损评分，改善了运动功能，减少了烟碱型乙酰胆碱受体（nAChR）α4β2免疫反应性细胞的数量，并增加了nAChRα7的细胞数量。此外，给予PF可抑制神经元凋亡并促进神经发生。
结论
PF挽救了神经功能缺损，其潜在机制是通过nAChRs抑制神经细胞凋亡和炎症。
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