检索结果-南通市图书馆

Sodium butyrate protects against focal cerebral ischemic injury through regulation of the nuclear receptor Nur77

分析化学 2021年

作者： MEN Li-Hui SONG Tong-Tong WANG Xi HUI Wen-Ting GU Yi-Wen DU Wen-Jing ZHANG Si-Wei CHEN Xia Department of Pharmacology， College of Basic Medical Sciences， Jilin University

Focal cerebral ischemia is a major cardiovascular disease that seriously threatens human health. Sodium butyrate has been identified as a neuromodulator in cerebral ischemia but the underlying mechanisms remain unclear. The present study aimed to clarify the neuronal anti-inflammatory mechanisms of sodium butyrate against focal cerebral ischemia. A focal cerebral ischemic rat model was established by administering sodium butyrate prior to middle cerebral artery occlusion (MCAO). The neuroprotective effects of sodium butyrate were evaluated 24 h after MCAO， using neurological score， infarction volume， and inflammatory biomarkers as the criteria. The expressions of nuclear receptor subfamily 4 group A1 (Nur77)， nod-like receptor protein 3 (NLRP3)， caspase-1 and interleukin-1β (IL-1β) in brain tissues were also analyzed. To explore the role of sodium butyrate in Nur77/NLRP3-mediated inflammatory response， oxygen and glucose deprivation (OGD)-stimulated HT22 cells were treated with sodium butyrate and siNur77. Sodium butyrate treatment significantly attenuated neurological impairment and neuroinflammation induced by cerebral ischemia. Sodium butyrate-mediated dysregulation of Nur77 expression and production of NLRP3-related inflammatory factors were observed in cerebral ischemia in vivo and in vitro. In addition， Nur77 was identified as a negative regulator of NLRP3 in HT22 cells under OGD. The results indicate that the anti-inflammatory effect of sodium butyrate was achieved by upregulating Nur77 expression， which subsequently suppressed neuronal NLRP3-mediated inflammatory response. Overall， sodium butyrate clearly has a neuroprotective effect against focal cerebral ischemia by modulating Nur77/NLRP3-mediated inflammatory response.

关键词： Sodium butyrate Focal cerebral ischemia Nuclear receptor subfamily 4 group A1 nod-like receptor protein 3 Inflammatory response

来源：

同方期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Effects of NLRP3 Inflammasome Mediated Pyroptosis on Cardiovascular Diseases and Intervention Mechanism of Chinese Medicine

引用

Chinese Journal of Integrative Medicine 2024年第5期30卷 468-479页

作者： ZHONG Yi LI Xin-yue LIANG Tian-jun DING Bao-zhu MA Ke-xin REN Wen-xuan LIANG Wen-jie College of Integrated Traditional Chinese and Western Medicine Hebei University of Chinese MedicineHebei Key Laboratory of Integrated Traditional Chinese and Western Medicine in Liver and Kidney DiseasesInstitute of Integrated Traditional Chinese and Western MedicineShijiazhuang 050200China Department of Cardiovascular Internal Medicine the Second Affiliated Hospital of Jiujiang UniversityJiujiangJiangxi Province 332000China Graduate School Hebei Medical UniversityShijiazhuang 050017China Rural Physician College Hebei Medical UniversityShijazhuang 050017China Medical Department the First Hospital of Hebei Medical UniversityShijiazhuang 050030China

Activation of the nod-like receptor protein 3(NLRP3)inflammasome signaling pathway is an important mechanism underlying myocardial pyroptosis and plays an important role in inflammatory damage to myocardial tissue in patients with cardiovascular diseases(CVDs),such as diabetic cardiomyopathy,ischemia/reperfusion injury,myocardial infarction,heart failure and *** RNAs(nc RNAs)are important regulatory *** Chinese medicine(CM)compounds,including their effective components,can regulate pyroptosis and exert myocardium-protecting *** mechanisms underlying this protection include inhibition of inflammasome protein expression,Toll-like receptor 4–NF-κB signal pathway activation,oxidative stress,endoplasmic reticulum stress(ERS),and mixed lineage kinase 3 expression and the regulation of silent information regulator *** NLRP3 protein is an important regulatory target for CVD prevention and treatment with *** the effects of the interventions mediated by CM and the related mechanisms provides new ideas and perspectives for CVD prevention and treatment.

关键词： pyroptosis cardiovascular diseases Chinese medicine nod-like receptor protein 3 mechanisms

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

NLRP3介导中性粒细胞募集参与脑梗死溶栓后出血转化

NLRP3介导中性粒细胞募集参与脑梗死溶栓后出血转化

引用

作者：郭志良南京大学

学位级别：硕士

目的重组组织型纤溶酶原激活剂(rtPA)静脉溶栓是急性脑梗死的首选治疗,溶栓后出血转化(HT)是其最严重的并发症。脑梗死溶栓后HT的主要病理特征是中性粒细胞募集,然而其启动及调节机制尚不明确。NLRP3(nod-like receptor protein 3)作为... 详细信息

目的重组组织型纤溶酶原激活剂(rtPA)静脉溶栓是急性脑梗死的首选治疗,溶栓后出血转化(HT)是其最严重的并发症。脑梗死溶栓后HT的主要病理特征是中性粒细胞募集,然而其启动及调节机制尚不明确。NLRP3(nod-like receptor protein 3)作为胞质内模式识别受体,在调节中性粒细胞募集中发挥重要作用。本研究旨在探讨NLRP3是否通过介导中性粒募集参与急性脑梗死rtPA溶栓HT,并同时证明脑梗死溶栓后调节中性粒细胞募集的中枢内关键分子可能为NLRP3。本研究期望为发现溶栓HT新的治疗方法提供理论依据。方法290-320 9 SD雄性大鼠进行局灶性血栓栓塞脑梗死模型,栓子注入后4小时给予rtPA溶栓治疗模拟临床出血转化。缺血前72小时右侧侧脑室注入表达NLRP3短发夹RNA(NLRP3 shRNA)的慢病毒敲减NLRP3。此外,脑缺血前给予兔抗大鼠中性粒血清抑制中性粒细胞。缺血后24小时进行梗死体积、水肿体积、神经功能缺损、出血转化、血脑屏障(BBB)完整性和脑内中性粒细胞募集情况评估。结果脑缺血后4小时延迟rtPA溶栓治疗促进NLRP3在神经元、小胶质细胞和内皮细胞表达,并促进BBB成分的退变,产生明显的出血转化。而慢病毒介导的短发夹RNA敲减NLRP3能够明显降低NLRP3表达,保护BBB以及减少出血转化,并且能够改善神经功能缺损;同时抑制NLRP3能够减少中性粒细募集。与NLRP3 shRNA类似,兔抗大鼠中性粒细胞血清同样减少延迟溶栓后出血评分及出血体积。而且,兔抗大鼠中性粒细胞血清与NLRP3 shRNA联用较单独应用并不增加其保护作用,这表明NLRP3可能通过募集中性粒细胞参与溶栓后HT。结论NLRP3可以通过调节中性粒细胞募集参与脑梗死溶栓后出血转化。

关键词：出血转化 nod-like receptor protein 3 中性粒细胞募集溶栓脑梗死

来源：

同方学位论文库评论

在线全文

同方学位论文库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：