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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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 |
work_keys_str_mv |
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