Glatiramer acetate does not protect from acute ischemic stroke in mice.

Peter Kraft, Kerstin Göbel, Sven G Meuth, Christoph Kleinschnitz
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引用次数: 12

Abstract

Background: The role of the immune system in the pathophysiology of acute ischemic stroke is increasingly recognized. However, targeted treatment strategies to modulate immunological pathways in stroke are still lacking. Glatiramer acetate is a multifaceted immunomodulator approved for the treatment of relapsing-remitting multiple sclerosis. Experimental studies suggest that glatiramer acetate might also work in other neuroinflammatory or neurodegenerative diseases apart from multiple sclerosis.

Findings: We evaluated the efficacy of glatiramer acetate in a mouse model of brain ischemia/reperfusion injury. 60 min of transient middle cerebral artery occlusion was induced in male C57Bl/6 mice. Pretreatment with glatiramer acetate (3.5 mg/kg bodyweight) 30 min before the induction of stroke did not reduce lesion volumes or improve functional outcome on day 1.

Conclusions: Glatiramer acetate failed to protect from acute ischemic stroke in our hands. Further studies are needed to assess the true therapeutic potential of glatiramer acetate and related immunomodulators in brain ischemia.

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醋酸格拉替默对小鼠急性缺血性中风无保护作用。
背景:免疫系统在急性缺血性脑卒中病理生理中的作用越来越被认识。然而,在脑卒中中调节免疫通路的靶向治疗策略仍然缺乏。醋酸格拉替默是一种多层免疫调节剂,被批准用于治疗复发缓解型多发性硬化症。实验研究表明,除了多发性硬化症外,醋酸格拉替雷默也可能对其他神经炎症或神经退行性疾病起作用。结果:我们评估了醋酸格拉替默对脑缺血再灌注损伤小鼠模型的疗效。雄性C57Bl/6小鼠短暂性大脑中动脉闭塞60 min。在脑卒中诱导前30分钟用醋酸格拉替默(3.5 mg/kg体重)预处理并没有减少病变体积或改善第1天的功能结局。结论:醋酸格拉替默对手部急性缺血性脑卒中没有保护作用。需要进一步的研究来评估醋酸格拉替默和相关免疫调节剂对脑缺血的真正治疗潜力。
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Hypoxia after stroke: a review of experimental and clinical evidence Therapeutic potential of the renin angiotensin system in ischaemic stroke Pathophysiology and management of reperfusion injury and hyperperfusion syndrome after carotid endarterectomy and carotid artery stenting. A pilot study evaluating the use of ABCD2 score in pre-hospital assessment of patients with suspected transient ischaemic attack: experience and lessons learned. Erratum to: Artery reopening is required for the neurorestorative effects of angiotensin modulation after experimental stroke.
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