• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

N-甲基-D-天冬氨酸受体部分拮抗剂氨基甲硫氨酸作为短暂性全脑缺血治疗药物的作用

The Role of NMDA Receptor Partial Antagonist, Carbamathione, as a Therapeutic Agent for Transient Global Ischemia.

作者信息

Modi Jigar Pravinchandra, Shen Wen, Menzie-Suderam Janet, Xu Hongyuan, Lin Chun-Hua, Tao Rui, Prentice Howard M, Schloss John, Wu Jang-Yen

机构信息

Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA.

Center of Complex Systems and Brain Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA.

出版信息

Biomedicines. 2023 Jul 3;11(7):1885. doi: 10.3390/biomedicines11071885.

DOI:10.3390/biomedicines11071885
PMID:37509524
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10377037/
Abstract

Carbamathione (Carb), an NMDA glutamate receptor partial antagonist, has potent neuroprotective functions against hypoxia- or ischemia-induced neuronal injury in cell- or animal-based stroke models. We used PC-12 cell cultures as a cell-based model and bilateral carotid artery occlusion (BCAO) for stroke. Whole-cell patch clamp recording in the mouse retinal ganglion cells was performed. Key proteins involved in apoptosis, endoplasmic reticulum (ER) stress, and heat shock proteins were analyzed using immunoblotting. Carb is effective in protecting PC12 cells against glutamate- or hypoxia-induced cell injury. Electrophysiological results show that Carb attenuates NMDA-mediated glutamate currents in the retinal ganglion cells, which results in activation of the AKT signaling pathway and increased expression of pro-cell survival biomarkers, e.g., Hsp 27, P-AKT, and Bcl2 and decreased expression of pro-cell death markers, e.g., Beclin 1, Bax, and Cleaved caspase 3, and ER stress markers, e.g., CHOP, IRE1, XBP1, ATF 4, and eIF2α. Using the BCAO animal stroke model, we found that Carb reduced the brain infarct volume and decreased levels of ER stress markers, GRP 78, CHOP, and at the behavioral level, e.g., a decrease in asymmetric turns and an increase in locomotor activity. These findings for Carb provide promising and rational strategies for stroke therapy.

摘要

卡巴谷胱甘肽(Carb)是一种N-甲基-D-天冬氨酸(NMDA)谷氨酸受体部分拮抗剂,在基于细胞或动物的中风模型中,对缺氧或缺血诱导的神经元损伤具有强大的神经保护功能。我们使用PC-12细胞培养物作为基于细胞的模型,并采用双侧颈动脉闭塞(BCAO)来模拟中风。对小鼠视网膜神经节细胞进行了全细胞膜片钳记录。使用免疫印迹法分析了参与细胞凋亡、内质网(ER)应激和热休克蛋白的关键蛋白。Carb可有效保护PC12细胞免受谷氨酸或缺氧诱导的细胞损伤。电生理结果表明,Carb可减弱视网膜神经节细胞中NMDA介导的谷氨酸电流,从而激活AKT信号通路,并增加细胞存活促进生物标志物(如热休克蛋白27、磷酸化AKT和Bcl2)的表达,同时降低细胞死亡标志物(如Beclin 1、Bax和裂解的半胱天冬酶3)以及内质网应激标志物(如CHOP、IRE1、XBP1、ATF 4和eIF2α)的表达。使用BCAO动物中风模型,我们发现Carb可减少脑梗死体积,并降低内质网应激标志物葡萄糖调节蛋白78(GRP 78)、CHOP的水平,在行为水平上,例如减少不对称转弯并增加运动活动。这些关于Carb的发现为中风治疗提供了有前景且合理的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/a8b4021097cb/biomedicines-11-01885-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/5928f5cf40c7/biomedicines-11-01885-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/6ace8d49082e/biomedicines-11-01885-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/323d95621a98/biomedicines-11-01885-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/9a982ea04147/biomedicines-11-01885-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/c591767ca354/biomedicines-11-01885-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/a553e317c7fd/biomedicines-11-01885-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/bd8ec92bc0cc/biomedicines-11-01885-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/297e42479cf2/biomedicines-11-01885-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/e2276e550a0c/biomedicines-11-01885-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/9674e769a77e/biomedicines-11-01885-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/a8b4021097cb/biomedicines-11-01885-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/5928f5cf40c7/biomedicines-11-01885-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/6ace8d49082e/biomedicines-11-01885-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/323d95621a98/biomedicines-11-01885-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/9a982ea04147/biomedicines-11-01885-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/c591767ca354/biomedicines-11-01885-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/a553e317c7fd/biomedicines-11-01885-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/bd8ec92bc0cc/biomedicines-11-01885-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/297e42479cf2/biomedicines-11-01885-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/e2276e550a0c/biomedicines-11-01885-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/9674e769a77e/biomedicines-11-01885-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9d/10377037/a8b4021097cb/biomedicines-11-01885-g011.jpg

相似文献

1
The Role of NMDA Receptor Partial Antagonist, Carbamathione, as a Therapeutic Agent for Transient Global Ischemia.N-甲基-D-天冬氨酸受体部分拮抗剂氨基甲硫氨酸作为短暂性全脑缺血治疗药物的作用
Biomedicines. 2023 Jul 3;11(7):1885. doi: 10.3390/biomedicines11071885.
2
Mode of action of granulocyte-colony stimulating factor (G-CSF) as a novel therapy for stroke in a mouse model.粒细胞集落刺激因子(G-CSF)作为一种新型治疗中风的方法在小鼠模型中的作用机制。
J Biomed Sci. 2020 Jan 6;27(1):19. doi: 10.1186/s12929-019-0597-7.
3
The mechanism of taurine protection against endoplasmic reticulum stress in an animal stroke model of cerebral artery occlusion and stroke-related conditions in primary neuronal cell culture.牛磺酸对脑动脉阻塞动物中风模型和原代神经元细胞培养中与中风相关条件的内质网应激的保护机制。
Adv Exp Med Biol. 2013;776:241-58. doi: 10.1007/978-1-4614-6093-0_23.
4
Comparison between single and combined post-treatment with S-Methyl-N,N-diethylthiolcarbamate sulfoxide and taurine following transient focal cerebral ischemia in rat brain.大鼠脑短暂性局灶性脑缺血后,S-甲基-N,N-二乙基硫代氨基甲酸盐亚砜与牛磺酸单一及联合治疗后的比较。
Neuroscience. 2015 Aug 6;300:460-73. doi: 10.1016/j.neuroscience.2015.05.042. Epub 2015 May 27.
5
Granulocyte-colony stimulating factor gene therapy as a novel therapeutics for stroke in a mouse model.粒细胞集落刺激因子基因治疗作为一种新型疗法在小鼠模型中治疗中风。
J Biomed Sci. 2020 Oct 30;27(1):99. doi: 10.1186/s12929-020-00692-5.
6
Mode of action of S-methyl-N, N-diethylthiocarbamate sulfoxide (DETC-MeSO) as a novel therapy for stroke in a rat model.S-甲基-N,N-二乙基硫代氨基甲酸盐亚砜(DETC-MeSO)作为大鼠中风新型治疗方法的作用机制
Mol Neurobiol. 2014 Oct;50(2):655-72. doi: 10.1007/s12035-014-8658-0. Epub 2014 Feb 28.
7
(-)-Clausenamide alleviated ER stress and apoptosis induced by OGD/R in primary neuron cultures.(-)-黄皮酰胺减轻原代神经元培养物中OGD/R诱导的内质网应激和细胞凋亡。
Neurol Res. 2020 Sep;42(9):730-738. doi: 10.1080/01616412.2020.1771040. Epub 2020 Jun 26.
8
Involvement of ER stress in retinal cell death.内质网应激与视网膜细胞死亡的关系。
Mol Vis. 2007 Apr 5;13:578-87.
9
Sigma-1 receptor protects against endoplasmic reticulum stress-mediated apoptosis in mice with cerebral ischemia/reperfusion injury.Sigma-1 受体可防止脑缺血/再灌注损伤小鼠内质网应激介导的细胞凋亡。
Apoptosis. 2019 Feb;24(1-2):157-167. doi: 10.1007/s10495-018-1495-2.
10
[Crosstalk between activating transcription factor 6 and the inositol-requiring enzyme 1-X-box binding protein 1 pathway in oxygen-glucose deprivation/reoxygenation-injured HT22 cells].[缺氧缺糖/复氧损伤的HT22细胞中激活转录因子6与肌醇需求酶1-X盒结合蛋白1信号通路之间的相互作用]
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2023 Mar;35(3):278-286. doi: 10.3760/cma.j.cn121430-20230228-00115.

引用本文的文献

1
Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review.脑缺氧诱导的分子改变及其对神经元和树突棘生理学的影响:全面综述。
Cell Mol Neurobiol. 2024 Aug 6;44(1):58. doi: 10.1007/s10571-024-01491-4.

本文引用的文献

1
Neuroinflammation: friend and foe for ischemic stroke.神经炎症:缺血性脑卒中的友敌。
J Neuroinflammation. 2019 Jul 10;16(1):142. doi: 10.1186/s12974-019-1516-2.
2
Nonhuman primate models of focal cerebral ischemia.局灶性脑缺血的非人灵长类动物模型。
Neural Regen Res. 2017 Feb;12(2):321-328. doi: 10.4103/1673-5374.200815.
3
Phosphoglycerate Kinase 1 Phosphorylates Beclin1 to Induce Autophagy.磷酸甘油酸激酶1使贝林1磷酸化以诱导自噬。
Mol Cell. 2017 Mar 2;65(5):917-931.e6. doi: 10.1016/j.molcel.2017.01.027. Epub 2017 Feb 23.
4
Ischemic stroke: experimental models and reality.缺血性脑卒中:实验模型与现实。
Acta Neuropathol. 2017 Feb;133(2):245-261. doi: 10.1007/s00401-017-1667-0. Epub 2017 Jan 7.
5
Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases.中风和神经退行性疾病中神经元抵御兴奋毒性、内质网应激及线粒体功能障碍的机制
Oxid Med Cell Longev. 2015;2015:964518. doi: 10.1155/2015/964518. Epub 2015 Oct 20.
6
Noninvasive tracking of gene transcript and neuroprotection after gene therapy.基因治疗后基因转录本的无创追踪与神经保护
Gene Ther. 2016 Jan;23(1):1-9. doi: 10.1038/gt.2015.81. Epub 2015 Jul 24.
7
Comparison between single and combined post-treatment with S-Methyl-N,N-diethylthiolcarbamate sulfoxide and taurine following transient focal cerebral ischemia in rat brain.大鼠脑短暂性局灶性脑缺血后,S-甲基-N,N-二乙基硫代氨基甲酸盐亚砜与牛磺酸单一及联合治疗后的比较。
Neuroscience. 2015 Aug 6;300:460-73. doi: 10.1016/j.neuroscience.2015.05.042. Epub 2015 May 27.
8
Altered lysosomal positioning affects lysosomal functions in a cellular model of Huntington's disease.溶酶体定位改变影响亨廷顿舞蹈症细胞模型中的溶酶体功能。
Eur J Neurosci. 2015 Aug;42(3):1941-51. doi: 10.1111/ejn.12957. Epub 2015 Jun 19.
9
Mechanisms and environmental factors that underlying the intensification of 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy)-induced serotonin syndrome in rats.3,4-亚甲基二氧甲基苯丙胺(摇头丸,MDMA)诱导大鼠血清素综合征加重的潜在机制和环境因素。
Psychopharmacology (Berl). 2015 Apr;232(7):1245-60. doi: 10.1007/s00213-014-3759-z. Epub 2014 Oct 11.
10
Inhibitory effect of ent-Sauchinone on amyloidogenesis via inhibition of STAT3-mediated NF-κB activation in cultured astrocytes and microglial BV-2 cells.内异贝壳杉烯酮通过抑制培养的星形胶质细胞和小胶质细胞BV-2中STAT3介导的NF-κB激活对淀粉样蛋白生成的抑制作用。
J Neuroinflammation. 2014 Jul 2;11:118. doi: 10.1186/1742-2094-11-118.