• 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

氧葡萄糖剥夺损伤的线粒体可通过激活 PI3K/Akt 通路和抑制氨氯地平 cam 酸盐的钙内流来恢复。

Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylate.

机构信息

Departments of Neurology, Hanyang University Guri Hospital, 11923, Guri, Korea.

Departments of Neurosurgery, Hanyang University Guri Hospital, 11923, Guri, Korea.

出版信息

Sci Rep. 2019 Oct 31;9(1):15717. doi: 10.1038/s41598-019-52083-y.

DOI:10.1038/s41598-019-52083-y
PMID:31673096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6823474/
Abstract

Amlodipine, a L-type calcium channel blocker, has been reported to have a neuroprotective effect in brain ischemia. Mitochondrial calcium overload leads to apoptosis of cells in neurologic diseases. We evaluated the neuroprotective effects of amlodipine camsylate (AC) on neural stem cells (NSCs) injured by oxygen glucose deprivation (OGD) with a focus on mitochondrial structure and function. NSCs were isolated from rodent embryonic brains. Effects of AC on cell viability, proliferation, level of free radicals, and expression of intracellular signaling proteins were assessed in OGD-injured NSCs. We also investigated the effect of AC on mitochondrial structure in NSCs under OGD by transmission electron microscopy. AC increased the viability and proliferation of NSCs. This beneficial effect of AC was achieved by strong protection of mitochondria. AC markedly enhanced the expression of mitochondrial biogenesis-related proteins and mitochondrial anti-apoptosis proteins. Together, our results indicate that AC protects OGD-injured NSCs by protecting mitochondrial structure and function. The results of the present study provide insight into the mechanisms underlying the protective effects of AC on NSCs.

摘要

氨氯地平是一种 L 型钙通道阻滞剂,据报道在脑缺血中有神经保护作用。线粒体钙超载导致神经疾病中的细胞凋亡。我们评估了氨氯地平 camsylate(AC)对氧葡萄糖剥夺(OGD)损伤的神经干细胞(NSC)的神经保护作用,重点关注线粒体的结构和功能。NSC 从啮齿动物胚胎脑中分离出来。在 OGD 损伤的 NSC 中评估 AC 对细胞活力、增殖、自由基水平和细胞内信号蛋白表达的影响。我们还通过透射电子显微镜研究了 AC 在 OGD 下对 NSC 中线粒体结构的影响。AC 增加了 NSC 的活力和增殖。AC 通过对线粒体的强烈保护来实现这种有益的效果。AC 显著增强了与线粒体生物发生相关的蛋白质和线粒体抗凋亡蛋白的表达。总之,我们的结果表明 AC 通过保护线粒体的结构和功能来保护 OGD 损伤的 NSC。本研究的结果为 AC 对 NSC 的保护作用的机制提供了深入的了解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/7d4732b7d3bb/41598_2019_52083_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/130579de0336/41598_2019_52083_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/3fba40c9259b/41598_2019_52083_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/38c1798f55b0/41598_2019_52083_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/edb734efb656/41598_2019_52083_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/80242d220552/41598_2019_52083_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/7d4732b7d3bb/41598_2019_52083_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/130579de0336/41598_2019_52083_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/3fba40c9259b/41598_2019_52083_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/38c1798f55b0/41598_2019_52083_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/edb734efb656/41598_2019_52083_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/80242d220552/41598_2019_52083_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c45/6823474/7d4732b7d3bb/41598_2019_52083_Fig6_HTML.jpg

相似文献

1
Mitochondria damaged by Oxygen Glucose Deprivation can be Restored through Activation of the PI3K/Akt Pathway and Inhibition of Calcium Influx by Amlodipine Camsylate.氧葡萄糖剥夺损伤的线粒体可通过激活 PI3K/Akt 通路和抑制氨氯地平 cam 酸盐的钙内流来恢复。
Sci Rep. 2019 Oct 31;9(1):15717. doi: 10.1038/s41598-019-52083-y.
2
Atorvastatin Rejuvenates Neural Stem Cells Injured by Oxygen-Glucose Deprivation and Induces Neuronal Differentiation Through Activating the PI3K/Akt and ERK Pathways.阿托伐他汀通过激活 PI3K/Akt 和 ERK 通路,使缺氧缺糖损伤的神经干细胞复苏并诱导其向神经元分化。
Mol Neurobiol. 2019 Apr;56(4):2964-2977. doi: 10.1007/s12035-018-1267-6. Epub 2018 Aug 3.
3
Neuroprotective effects of amlodipine besylate and benidipine hydrochloride on oxidative stress-injured neural stem cells.苯磺酸氨氯地平和盐酸贝尼地平对氧化应激损伤神经干细胞的神经保护作用。
Brain Res. 2014 Mar 10;1551:1-12. doi: 10.1016/j.brainres.2014.01.016. Epub 2014 Jan 16.
4
Telmisartan Inhibits the NLRP3 Inflammasome by Activating the PI3K Pathway in Neural Stem Cells Injured by Oxygen-Glucose Deprivation.替米沙坦通过激活神经干细胞中 PI3K 通路抑制氧糖剥夺损伤诱导的 NLRP3 炎症小体。
Mol Neurobiol. 2021 Apr;58(4):1806-1818. doi: 10.1007/s12035-020-02253-1. Epub 2021 Jan 6.
5
GRP78 Promotes Neural Stem Cell Antiapoptosis and Survival in Response to Oxygen-Glucose Deprivation (OGD)/Reoxygenation through PI3K/Akt, ERK1/2, and NF-B/p65 Pathways.GRP78 通过 PI3K/Akt、ERK1/2 和 NF-κB/p65 通路促进神经干细胞在氧葡萄糖剥夺(OGD)/复氧后抗凋亡和存活。
Oxid Med Cell Longev. 2018 Apr 10;2018:3541807. doi: 10.1155/2018/3541807. eCollection 2018.
6
Pyrroloquinoline quinone inhibits oxygen/glucose deprivation-induced apoptosis by activating the PI3K/AKT pathway in cardiomyocytes.吡咯喹啉醌通过激活心肌细胞中的 PI3K/AKT 通路抑制氧/葡萄糖剥夺诱导的细胞凋亡。
Mol Cell Biochem. 2014 Jan;386(1-2):107-15. doi: 10.1007/s11010-013-1849-6. Epub 2013 Oct 11.
7
Inhibition of the NLRP3 Inflammasome Activation/Assembly through the Activation of the PI3K Pathway by Naloxone Protects Neural Stem Cells from Ischemic Condition.纳洛酮通过激活 PI3K 通路抑制 NLRP3 炎性小体的激活/组装,从而保护神经干细胞免受缺血性损伤。
Mol Neurobiol. 2023 Sep;60(9):5330-5342. doi: 10.1007/s12035-023-03418-4. Epub 2023 Jun 10.
8
UBIAD1 protects against oxygen-glucose deprivation/reperfusion-induced multiple subcellular organelles injury through PI3K/AKT pathway in N2A cells.UBIAD1 通过 PI3K/AKT 通路保护 N2A 细胞免受氧葡萄糖剥夺/再灌注诱导的多种亚细胞细胞器损伤。
J Cell Physiol. 2018 Sep;233(9):7480-7496. doi: 10.1002/jcp.26602. Epub 2018 Apr 16.
9
Neuroprotective effects of astaxanthin against oxygen and glucose deprivation damage via the PI3K/Akt/GSK3β/Nrf2 signalling pathway in vitro.虾青素通过体外 PI3K/Akt/GSK3β/Nrf2 信号通路对氧葡萄糖剥夺损伤的神经保护作用。
J Cell Mol Med. 2020 Aug;24(16):8977-8985. doi: 10.1111/jcmm.15531. Epub 2020 Jun 21.
10
CXCL16 protects against oxygen and glucose deprivation-induced injury in human microvascular endothelial cells-1: Potential role in ischemic stroke.CXCL16 可保护人微血管内皮细胞-1 免受缺氧和葡萄糖剥夺诱导的损伤-1:在缺血性脑卒中的潜在作用。
J Cell Physiol. 2019 Nov;234(11):20149-20160. doi: 10.1002/jcp.28616. Epub 2019 Apr 3.

引用本文的文献

1
Catalpol Protects Against Retinal Ischemia Through Antioxidation, Anti-Ischemia, Downregulation of β-Catenin, VEGF, and Angiopoietin-2: In Vitro and In Vivo Studies.梓醇通过抗氧化、抗缺血、下调β-连环蛋白、血管内皮生长因子和血管生成素-2对视网膜缺血起到保护作用:体外和体内研究
Int J Mol Sci. 2025 Apr 24;26(9):4019. doi: 10.3390/ijms26094019.
2
Exploring Potential Medications for Alzheimer's Disease with Psychosis by Integrating Drug Target Information into Deep Learning Models: A Data-Driven Approach.通过将药物靶点信息整合到深度学习模型中探索用于伴有精神病的阿尔茨海默病的潜在药物:一种数据驱动方法
Int J Mol Sci. 2025 Feb 14;26(4):1617. doi: 10.3390/ijms26041617.
3

本文引用的文献

1
Candesartan Restores the Amyloid Beta-Inhibited Proliferation of Neural Stem Cells by Activating the Phosphatidylinositol 3-Kinase Pathway.坎地沙坦通过激活磷脂酰肌醇3-激酶途径恢复淀粉样β蛋白抑制的神经干细胞增殖。
Dement Neurocogn Disord. 2017 Sep;16(3):64-71. doi: 10.12779/dnd.2017.16.3.64. Epub 2017 Sep 30.
2
Linalyl acetate prevents hypertension-related ischemic injury.乙酸芳樟酯可预防高血压相关的缺血性损伤。
PLoS One. 2018 May 25;13(5):e0198082. doi: 10.1371/journal.pone.0198082. eCollection 2018.
3
Neuroprotective mechanisms of miR-124 activating PI3K/Akt signaling pathway in ischemic stroke.
Validation of L-type calcium channel blocker amlodipine as a novel ADHD treatment through cross-species analysis, drug-target Mendelian randomization, and clinical evidence from medical records.
通过跨物种分析、药物靶点孟德尔随机化以及病历临床证据验证L型钙通道阻滞剂氨氯地平作为一种新型多动症治疗药物的有效性。
Neuropsychopharmacology. 2025 Jun;50(7):1145-1155. doi: 10.1038/s41386-025-02062-x. Epub 2025 Feb 14.
4
Gene ontology defines pre-post- hatch energy dynamics in the complexus muscle of broiler chickens.基因本体论定义了肉鸡复杂肌肉中孵化前后的能量动态。
BMC Genomics. 2024 Dec 4;25(1):1180. doi: 10.1186/s12864-024-11103-6.
5
Inhibition of the NLRP3 Inflammasome Activation/Assembly through the Activation of the PI3K Pathway by Naloxone Protects Neural Stem Cells from Ischemic Condition.纳洛酮通过激活 PI3K 通路抑制 NLRP3 炎性小体的激活/组装,从而保护神经干细胞免受缺血性损伤。
Mol Neurobiol. 2023 Sep;60(9):5330-5342. doi: 10.1007/s12035-023-03418-4. Epub 2023 Jun 10.
6
Posttreatment with Ospemifene Attenuates Hypoxia- and Ischemia-Induced Apoptosis in Primary Neuronal Cells via Selective Modulation of Estrogen Receptors.奥昔布宁治疗通过选择性调节雌激素受体减轻原代神经元细胞缺氧缺血诱导的细胞凋亡。
Neurotox Res. 2023 Aug;41(4):362-379. doi: 10.1007/s12640-023-00644-5. Epub 2023 May 2.
7
Mitochondria-containing extracellular vesicles (EV) reduce mouse brain infarct sizes and EV/HSP27 protect ischemic brain endothelial cultures.含线粒体的细胞外囊泡(EV)可减小小鼠脑梗死体积,EV/HSP27 可保护缺血性脑内皮细胞培养物。
J Control Release. 2023 Feb;354:368-393. doi: 10.1016/j.jconrel.2023.01.025. Epub 2023 Jan 18.
8
Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed.常见心血管药物的线粒体效应:好、坏及混合。
Int J Mol Sci. 2022 Nov 7;23(21):13653. doi: 10.3390/ijms232113653.
9
PDIA3 inhibits mitochondrial respiratory function in brain endothelial cells and C. elegans through STAT3 signaling and decreases survival after OGD.PDIA3 通过 STAT3 信号抑制脑内皮细胞和秀丽隐杆线虫中的线粒体呼吸功能,并降低 OGD 后的存活率。
Cell Commun Signal. 2021 Dec 18;19(1):119. doi: 10.1186/s12964-021-00794-z.
10
Melatonin reshapes the mitochondrial network and promotes intercellular mitochondrial transfer via tunneling nanotubes after ischemic-like injury in hippocampal HT22 cells.缺血样损伤后,褪黑素重塑线粒体网络,并通过隧道纳米管促进细胞间线粒体转移。
J Pineal Res. 2021 Aug;71(1):e12747. doi: 10.1111/jpi.12747. Epub 2021 Jun 14.
miR-124通过激活PI3K/Akt信号通路在缺血性卒中中的神经保护机制
Exp Ther Med. 2017 Jun;13(6):3315-3318. doi: 10.3892/etm.2017.4424. Epub 2017 May 4.
4
Amlodipine, an L-type calcium channel blocker, protects against chlorpromazine-induced neurobehavioural deficits in mice.氨氯地平,一种L型钙通道阻滞剂,可预防氯丙嗪诱导的小鼠神经行为缺陷。
Fundam Clin Pharmacol. 2017 Jun;31(3):329-339. doi: 10.1111/fcp.12267. Epub 2017 Feb 20.
5
Mitochondrial dynamics as regulators of cancer biology.线粒体动力学作为癌症生物学的调节因子
Cell Mol Life Sci. 2017 Jun;74(11):1999-2017. doi: 10.1007/s00018-016-2451-3. Epub 2017 Jan 12.
6
Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury.一氧化碳对创伤性脑损伤中周细胞和神经发生的双重影响。
Nat Med. 2016 Nov;22(11):1335-1341. doi: 10.1038/nm.4188. Epub 2016 Sep 26.
7
Bcl-2 proteins and calcium signaling: complexity beneath the surface.Bcl-2蛋白与钙信号传导:表面之下的复杂性
Oncogene. 2016 Sep 29;35(39):5079-92. doi: 10.1038/onc.2016.31. Epub 2016 Mar 14.
8
Effect of L-type calcium channel blocker (amlodipine) on myocardial iron deposition in patients with thalassaemia with moderate-to-severe myocardial iron deposition: protocol for a randomised, controlled trial.L型钙通道阻滞剂(氨氯地平)对中重度心肌铁沉积的地中海贫血患者心肌铁沉积的影响:一项随机对照试验方案
BMJ Open. 2014 Dec 8;4(12):e005360. doi: 10.1136/bmjopen-2014-005360.
9
Neuroprotective effects of amlodipine besylate and benidipine hydrochloride on oxidative stress-injured neural stem cells.苯磺酸氨氯地平和盐酸贝尼地平对氧化应激损伤神经干细胞的神经保护作用。
Brain Res. 2014 Mar 10;1551:1-12. doi: 10.1016/j.brainres.2014.01.016. Epub 2014 Jan 16.
10
Oxygen glucose deprivation (OGD)/re-oxygenation-induced in vitro neuronal cell death involves mitochondrial cyclophilin-D/P53 signaling axis.氧葡萄糖剥夺(OGD)/再复氧诱导的体外神经元细胞死亡涉及线粒体亲环素-D/P53 信号轴。
Neurochem Res. 2013 Apr;38(4):705-13. doi: 10.1007/s11064-013-0968-5. Epub 2013 Jan 16.