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

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 necrop...

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Main Authors: Shehong Zhang, Yuyang Wang, Dake Li, Junfa Wu, Wen Si, Yi Wu
Format: Article
Language:English
Published: MDPI AG 2016-07-01
Series:Medicines
Subjects:
Online Access:http://www.mdpi.com/2305-6320/3/3/16
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spelling doaj-f8d19b1517764774880b5e3212d383502020-11-25T00:59:19ZengMDPI AGMedicines2305-63202016-07-01331610.3390/medicines3030016medicines3030016Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke MiceShehong Zhang0Yuyang Wang1Dake Li2Junfa Wu3Wen Si4Yi Wu5Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, ChinaDepartment of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, ChinaMultiple 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.http://www.mdpi.com/2305-6320/3/3/16necroptosisischemiacognitioninflammation
collection DOAJ
language English
format Article
sources DOAJ
author Shehong Zhang
Yuyang Wang
Dake Li
Junfa Wu
Wen Si
Yi Wu
spellingShingle Shehong Zhang
Yuyang Wang
Dake Li
Junfa Wu
Wen Si
Yi Wu
Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
Medicines
necroptosis
ischemia
cognition
inflammation
author_facet Shehong Zhang
Yuyang Wang
Dake Li
Junfa Wu
Wen Si
Yi Wu
author_sort Shehong Zhang
title Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
title_short Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
title_full Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
title_fullStr Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
title_full_unstemmed Necrostatin-1 Attenuates Inflammatory Response and Improves Cognitive Function in Chronic Ischemic Stroke Mice
title_sort necrostatin-1 attenuates inflammatory response and improves cognitive function in chronic ischemic stroke mice
publisher MDPI AG
series Medicines
issn 2305-6320
publishDate 2016-07-01
description 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.
topic necroptosis
ischemia
cognition
inflammation
url http://www.mdpi.com/2305-6320/3/3/16
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