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Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice

1
Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China
2
Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China
*
Author to whom correspondence should be addressed.
Academic Editor: Gerhard Litscher
Medicines 2016, 3(3), 16; https://doi.org/10.3390/medicines3030016
Received: 30 March 2016 / Revised: 18 June 2016 / Accepted: 21 June 2016 / Published: 1 July 2016
Multiple cell death is involved in ischemic brain injury. Necroptosis, a recently reported cell death, may be the most suitable cell death mechanism in a subpopulation of neurons under ischemic injury. It reported that a small molecule, necrostatin-1 (Nec-1), has a potent inhibitory effect on necroptotic cell death in vivo and in vitro. The aim of the current study was to investigate the role of Nec-1 on cognitive function in chronic ischemic stroke mice induced by bilateral common carotid artery stenosis (BCAS). Here, 12-week-old C57BL/6 mice received intragastric administration with Nec-1 or vehicle for two weeks after stroke, and then, the effect and possible mechanism were determined. We demonstrated that inhibition of necroptosis prevented cognitive impairment and reduced inflammatory response in the ischemic brain injury mouse model. These data suggested that inhibition of necroptosis provided a potential therapeutic option for cognitive rehabilitation in chronic ischemic stroke. View Full-Text
Keywords: necroptosis; ischemia; cognition; inflammation necroptosis; ischemia; cognition; inflammation
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Zhang, S.; Wang, Y.; Li, D.; Wu, J.; Si, W.; Wu, Y. Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice. Medicines 2016, 3, 16.

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