文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

中性粒细胞膜衍生的纳米颗粒通过抑制钙超载和清除 ROS 来保护创伤性脑损伤。

Neutrophil membrane-derived nanoparticles protect traumatic brain injury via inhibiting calcium overload and scavenging ROS.

机构信息

Department of Nuclear Medicine, Daping Hospital, Army Medical University, Chongqing, 400042, China.

College of Basic Medicine, Chongqing Medical University, Chongqing, 400016, China.

出版信息

J Nanobiotechnology. 2024 Aug 12;22(1):477. doi: 10.1186/s12951-024-02753-5.

DOI:10.1186/s12951-024-02753-5
PMID:39135044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11320991/
Abstract

The secondary injury is more serious after traumatic brain injury (TBI) compared with primary injury. Release of excessive reactive oxygen species (ROS) and Ca influx at the damaged site trigger the secondary injury. Herein, a neutrophil-like cell membrane-functionalized nanoparticle was developed to prevent ROS-associated secondary injury. NCM@MP was composed of three parts: (1) Differentiated neutrophil-like cell membrane (NCM) was synthesized, with inflammation-responsive ability to achieve effective targeting and to increase the retention time of MnO and nimodipine (MP) in deep injury brain tissue via C-X-C chemokine receptor type 4, integrin beta 1 and macrophage antigen-1. (2) Nimodipine was used to inhibit Ca influx, eliminating the ROS at source. (3) MnO further eradicated the existing ROS. In addition, NCM@MP also exhibited desirable properties for T enhanced imaging and low toxicity which may serve as promising multifunctional nanoplatforms for precise therapies. In our study, NCM@MP obviously alleviated oxidative stress response, reduced neuroinflammation, protected blood-brain barrier integrity, relieved brain edema, promoted the regeneration of neurons, and improved the cognition of TBI mice. This study provides a promising TBI management to relieve the secondary spread of damage.

摘要

创伤性脑损伤 (TBI) 后的二次损伤比原发性损伤更为严重。损伤部位过量活性氧 (ROS) 和 Ca 内流的释放会引发二次损伤。在此，开发了一种具有中性粒细胞样细胞膜功能化的纳米颗粒，以防止与 ROS 相关的二次损伤。NCM@MP 由三部分组成：(1) 合成分化的中性粒细胞样细胞膜 (NCM)，具有炎症反应能力，通过 C-X-C 趋化因子受体 4、整合素 β1 和巨噬细胞抗原-1 实现有效靶向，并增加 MnO 和尼莫地平 (MP) 在深部损伤脑组织中的保留时间。(2) 尼莫地平用于抑制 Ca 内流，从源头上消除 ROS。(3) MnO 进一步消除现有的 ROS。此外，NCM@MP 还表现出用于 T 增强成像的理想特性和低毒性，这使其可能成为用于精确治疗的有前途的多功能纳米平台。在我们的研究中，NCM@MP 明显减轻了氧化应激反应，减轻了神经炎症，保护了血脑屏障的完整性，缓解了脑水肿，促进了神经元的再生，并改善了 TBI 小鼠的认知能力。本研究为 TBI 管理提供了一种有前途的方法，以减轻继发性损伤的扩散。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/703c45771265/12951_2024_2753_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/fe32eec09acf/12951_2024_2753_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/3fc3227df952/12951_2024_2753_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/2c7a4a7597bb/12951_2024_2753_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/e774a28b465b/12951_2024_2753_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/2b89525ca299/12951_2024_2753_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/703c45771265/12951_2024_2753_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/fe32eec09acf/12951_2024_2753_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/3fc3227df952/12951_2024_2753_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/2c7a4a7597bb/12951_2024_2753_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/e774a28b465b/12951_2024_2753_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/2b89525ca299/12951_2024_2753_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f573/11320991/703c45771265/12951_2024_2753_Fig6_HTML.jpg

相似文献

[1]
Neutrophil membrane-derived nanoparticles protect traumatic brain injury via inhibiting calcium overload and scavenging ROS.

J Nanobiotechnology. 2024-8-12

[2]
A Novel Targeted Nanoparticle for Traumatic Brain Injury Treatment: Combined Effect of ROS Depletion and Calcium Overload Inhibition.

Adv Healthc Mater. 2022-6

[3]
Irisin Rescues Blood-Brain Barrier Permeability following Traumatic Brain Injury and Contributes to the Neuroprotection of Exercise in Traumatic Brain Injury.

Oxid Med Cell Longev. 2021

[4]
Tachykinin NK1 receptor antagonist L-733,060 and substance P deletion exert neuroprotection through inhibiting oxidative stress and cell death after traumatic brain injury in mice.

Int J Biochem Cell Biol. 2018-12-26

[5]
Logic "AND Gate Circuit" Based Mussel Inspired Polydopamine Nanocomposite as Bioactive Antioxidant for Management of Oxidative Stress and Neurogenesis in Traumatic Brain Injury.

ACS Appl Mater Interfaces. 2024-7-17

[6]
Cordycepin confers long-term neuroprotection via inhibiting neutrophil infiltration and neuroinflammation after traumatic brain injury.

J Neuroinflammation. 2021-6-15

[7]
Effective treatment of traumatic brain injury by injection of a selenium-containing ointment.

Acta Biomater. 2024-10-1

[8]
Inhibition of Heat Shock Protein 90 Attenuates the Damage of Blood-Brain Barrier Integrity in Traumatic Brain Injury Mouse Model.

Oxid Med Cell Longev. 2022

[9]
Rhein and rhubarb similarly protect the blood-brain barrier after experimental traumatic brain injury via gp91 subunit of NADPH oxidase/ROS/ERK/MMP-9 signaling pathway.

Sci Rep. 2016-11-30

[10]
Time courses of post-injury mitochondrial oxidative damage and respiratory dysfunction and neuronal cytoskeletal degradation in a rat model of focal traumatic brain injury.

Neurochem Int. 2017-3-23

引用本文的文献

[1]
Decreased IL-33 in the brain following repetitive mild traumatic brain injury contributes to cognitive impairment by inhibiting microglial phagocytosis.

Mil Med Res. 2025-8-5

[2]
β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.

Cell Commun Signal. 2025-2-8

[3]
Size effect-based improved antioxidant activity of selenium nanoparticles regulating Anti-PI3K-mTOR and Ras-MEK pathways for treating spinal cord injury to avoid hormone shock-induced immunosuppression.

J Nanobiotechnology. 2025-1-16

本文引用的文献

[1]
SHED-derived exosomes attenuate trigeminal neuralgia after CCI of the infraorbital nerve in mice via the miR-24-3p/IL-1R1/p-p38 MAPK pathway.

J Nanobiotechnology. 2023-11-29

[2]
Modified Xiaoyao San reverses lipopolysaccharide-induced depression-like behavior through suppressing microglia M1 polarization via enhancing autophagy involved in PI3K/Akt/mTOR pathway in mice.

J Ethnopharmacol. 2023-10-28

[3]
Alpinetin inhibits neuroinflammation and neuronal apoptosis via targeting the JAK2/STAT3 signaling pathway in spinal cord injury.

CNS Neurosci Ther. 2023-4

[4]
Fewer COVID-19 Neurological Complications with Dexamethasone and Remdesivir.

Ann Neurol. 2023-1

[5]
Improved gliotransmission by increasing intracellular Ca via TRPV1 on multi-walled carbon nanotube platforms.

J Nanobiotechnology. 2022-8-11

[6]
Pathogenesis and management of traumatic brain injury (TBI): role of neuroinflammation and anti-inflammatory drugs.

Inflammopharmacology. 2022-8

[7]
Intrinsically Bioactive Manganese-Eumelanin Nanocomposites Mediated Antioxidation and Anti-Neuroinflammation for Targeted Theranostics of Traumatic Brain Injury.

Adv Healthc Mater. 2022-8

[8]
A Novel Targeted Nanoparticle for Traumatic Brain Injury Treatment: Combined Effect of ROS Depletion and Calcium Overload Inhibition.

Adv Healthc Mater. 2022-6

[9]
TREM2 Ameliorates Lipopolysaccharide-Induced Oxidative Stress Response and Neuroinflammation by Promoting Sirtuin3 in BV2 Cells.

Neurotox Res. 2022-2

[10]
Antioxidant therapies in traumatic brain injury.

Neurochem Int. 2022-1

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索