Overexpressing SIRT6 can Attenuate the Injury of Intracerebral Hemorrhage by Down-Regulating NF-kB.

IF 3.9 4区 医学 Q2 NEUROSCIENCES NeuroMolecular Medicine Pub Date : 2023-03-01 Epub Date: 2022-06-29 DOI:10.1007/s12017-022-08715-0
Jing Cheng, Yan-Qin Fan, Wen-Fei Zhang, Guo Zhang, Kuo Zeng, Zhang Ye, Dan Zhao, Li-Quan Wu, Zhi-Biao Chen
{"title":"Overexpressing SIRT6 can Attenuate the Injury of Intracerebral Hemorrhage by Down-Regulating NF-kB.","authors":"Jing Cheng, Yan-Qin Fan, Wen-Fei Zhang, Guo Zhang, Kuo Zeng, Zhang Ye, Dan Zhao, Li-Quan Wu, Zhi-Biao Chen","doi":"10.1007/s12017-022-08715-0","DOIUrl":null,"url":null,"abstract":"<p><p>Sirtuin-6 (SIRT6), a member of the sirtuins family of NAD ( +) dependent deacetylases, has been shown to have beneficial effects in ischemic stroke. However, the role of SIRT6 in intracerebral haemorrhage (ICH) has not reported. We observed that SIRT6 expression was down-regulated in human ICH patients and down-regulated in ICH-induced rat cortical neurons. We subsequently found that SIRT6 overexpression reduced brain tissue damage and increased neuronal survival in the ICH model of rats and hemin-induced cortical neurons. Our further study found that overexpression of SIRT6 can reduce inflammatory response by down-regulating the expression of NF-kB and thus promote the recovery of neurological function in ICH animals. In conclusion, SIRT6 can inhibit the expression of NF-kB and plays a neuroprotective role in ICH by inhibiting the NF-kB-mediated inflammatory response.SIRT6 could be a novel therapeutic target for ICH.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"25 1","pages":"53-63"},"PeriodicalIF":3.9000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"NeuroMolecular Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12017-022-08715-0","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/6/29 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Sirtuin-6 (SIRT6), a member of the sirtuins family of NAD ( +) dependent deacetylases, has been shown to have beneficial effects in ischemic stroke. However, the role of SIRT6 in intracerebral haemorrhage (ICH) has not reported. We observed that SIRT6 expression was down-regulated in human ICH patients and down-regulated in ICH-induced rat cortical neurons. We subsequently found that SIRT6 overexpression reduced brain tissue damage and increased neuronal survival in the ICH model of rats and hemin-induced cortical neurons. Our further study found that overexpression of SIRT6 can reduce inflammatory response by down-regulating the expression of NF-kB and thus promote the recovery of neurological function in ICH animals. In conclusion, SIRT6 can inhibit the expression of NF-kB and plays a neuroprotective role in ICH by inhibiting the NF-kB-mediated inflammatory response.SIRT6 could be a novel therapeutic target for ICH.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
过表达 SIRT6 可通过下调 NF-kB 减轻脑出血的损伤
Sirtuin 6(SIRT6)是依赖于 NAD ( +) 的去乙酰化酶 sirtuins 家族的成员,已被证明对缺血性中风有益处。然而,SIRT6 在脑内出血(ICH)中的作用尚未见报道。我们观察到 SIRT6 在人类 ICH 患者中表达下调,在 ICH 诱导的大鼠皮质神经元中表达下调。随后我们发现,在大鼠 ICH 模型和海明诱导的大脑皮层神经元中,SIRT6 的过表达可减少脑组织损伤,提高神经元存活率。我们的进一步研究发现,过表达 SIRT6 可通过下调 NF-kB 的表达来减轻炎症反应,从而促进 ICH 动物神经功能的恢复。总之,SIRT6 可抑制 NF-kB 的表达,并通过抑制 NF-kB 介导的炎症反应在 ICH 中发挥神经保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
NeuroMolecular Medicine
NeuroMolecular Medicine 医学-神经科学
CiteScore
7.10
自引率
0.00%
发文量
33
审稿时长
>12 weeks
期刊介绍: NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.
期刊最新文献
Pterostilbene Orchestrates Synaptic Remodeling and Mitochondrial Functional Reconstitution to Attenuate Ischemic Vascular Dementia. Montelukast Modulates MPTP-induced Ferroptosis and Neuroinflammation Linked To the GPX4/ACSL4/5-LOX Pathway. Retraction Note: 5‑N‑ethyl Carboxamidoadenosine Stimulates Adenosine‑2b Receptor‑Mediated Mitogen‑Activated Protein Kinase Pathway to Improve Brain Mitochondrial Function in Amyloid Beta‑Induced Cognitive Deficit Mice. Searching for New Possible Peripheral Biomarkers of Cognitive Decline in Down Syndrome: The Role of IL-18 Pathway and its Interaction with TGF-β1 and TNF-α. Simvastatin Ameliorates Lipid Metabolism-Mediated Endothelial Inflammation and Tight Junction Impairment in Chronic Cerebral Hypoperfusion.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1