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含磷脂酰丝氨酸的脂质体可促进缺血性损伤后视网膜神经元的最大存活。

Phosphatidylserine-containing liposomes promote maximal survival of retinal neurons after ischemic injury.

作者信息

Dvoriantchikova Galina, Agudelo Christian, Hernandez Eleut, Shestopalov Valery I, Ivanov Dmitry

机构信息

Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.

出版信息

J Cereb Blood Flow Metab. 2009 Nov;29(11):1755-9. doi: 10.1038/jcbfm.2009.95. Epub 2009 Jul 15.

Abstract

We investigated the systemic effect of liposomes bearing apoptotic signals on the level of inflammation and neuronal death induced by ischemia-reperfusion (IR). Using a model of retinal ischemia, we showed that treatment with phosphatidylserine (PS) and phosphatidylcholine (PC) liposomes significantly reduced the expression of proinflammatory genes, including that of Il1b, Il6, Ccl2, Ccl5, Cxcl10, and Icam1, 24 h after reperfusion. Phosphatidylserine liposome treatment was the most efficient and correlated with significantly reduced neuronal death in the retina 7 days after reperfusion. The results of our study indicate that therapeutic strategy based on mimicking a systemic increase in apoptotic signaling can significantly reduce central nervous system damage induced by IR and improve neurologic outcome.

摘要

我们研究了携带凋亡信号的脂质体对缺血再灌注(IR)诱导的炎症水平和神经元死亡的全身影响。利用视网膜缺血模型,我们发现用磷脂酰丝氨酸(PS)和磷脂酰胆碱(PC)脂质体处理可在再灌注后24小时显著降低促炎基因的表达,包括Il1b、Il6、Ccl2、Ccl5、Cxcl10和Icam1的表达。磷脂酰丝氨酸脂质体处理最为有效,且与再灌注7天后视网膜中神经元死亡显著减少相关。我们的研究结果表明,基于模拟凋亡信号全身性增加的治疗策略可显著降低IR诱导的中枢神经系统损伤并改善神经学结果。

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