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氧化应激标志物对缺血性脑卒中患者的影响。

The Influence of Oxidative Stress Markers in Patients with Ischemic Stroke.

机构信息

Department of Medical Biology and Biochemistry, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Karlowicza 24, 85-092 Bydgoszcz, Poland.

Department of Organic Chemistry, Faculty of Chemistry, Nicolaus Copernicus University, Gagarina 7, 87-100 Torun, Poland.

出版信息

Biomolecules. 2024 Sep 6;14(9):1130. doi: 10.3390/biom14091130.


DOI:10.3390/biom14091130
PMID:39334896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11430825/
Abstract

Stroke is the second leading cause of death worldwide, and its incidence is rising rapidly. Acute ischemic stroke is a subtype of stroke that accounts for the majority of stroke cases and has a high mortality rate. An effective treatment for stroke is to minimize damage to the brain's neural tissue by restoring blood flow to decreased perfusion areas of the brain. Many reports have concluded that both oxidative stress and excitotoxicity are the main pathological processes associated with ischemic stroke. Current measures to protect the brain against serious damage caused by stroke are insufficient. For this reason, it is important to investigate oxidative and antioxidant strategies to reduce oxidative damage. This review focuses on studies assessing the concentration of oxidative stress biomarkers and the level of antioxidants (enzymatic and non-enzymatic) and their impact on the clinical prognosis of patients after stroke. Mechanisms related to the production of ROS/RNS and the role of oxidative stress in the pathogenesis of ischemic stroke are presented, as well as new therapeutic strategies aimed at reducing the effects of ischemia and reperfusion.

摘要

中风是全球第二大致死原因,其发病率正在迅速上升。急性缺血性中风是中风的一种亚型,占中风病例的大多数,死亡率很高。治疗中风的有效方法是通过恢复大脑灌注减少区域的血流来最小化对大脑神经组织的损伤。许多报告得出结论,氧化应激和兴奋毒性都是与缺血性中风相关的主要病理过程。目前保护大脑免受中风严重损伤的措施还不够。因此,研究氧化和抗氧化策略以减少氧化损伤非常重要。本综述重点介绍了评估氧化应激生物标志物浓度和抗氧化剂(酶和非酶)水平及其对中风后患者临床预后影响的研究。本文介绍了与 ROS/RNS 产生相关的机制以及氧化应激在缺血性中风发病机制中的作用,以及旨在减少缺血和再灌注影响的新治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/38422871da5e/biomolecules-14-01130-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/7f90397afc27/biomolecules-14-01130-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/5067a38d4fa2/biomolecules-14-01130-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/fe2521a6d32b/biomolecules-14-01130-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/cdb616ba28b5/biomolecules-14-01130-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/06b9b727ca1b/biomolecules-14-01130-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/9684a46551dd/biomolecules-14-01130-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/9b56239a5e13/biomolecules-14-01130-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/8a8b694493e7/biomolecules-14-01130-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/38422871da5e/biomolecules-14-01130-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/7f90397afc27/biomolecules-14-01130-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/5067a38d4fa2/biomolecules-14-01130-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/fe2521a6d32b/biomolecules-14-01130-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/cdb616ba28b5/biomolecules-14-01130-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/06b9b727ca1b/biomolecules-14-01130-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/9684a46551dd/biomolecules-14-01130-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/9b56239a5e13/biomolecules-14-01130-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/8a8b694493e7/biomolecules-14-01130-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ef9/11430825/38422871da5e/biomolecules-14-01130-g009.jpg

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本文引用的文献

[1]
Ecdysterone improves oxidative damage induced by acute ischemic stroke via inhibiting ferroptosis in neurons through ACSL4.

J Ethnopharmacol. 2024-9-15

[2]
Melatonin ameliorates retinal ganglion cell senescence and apoptosis in a SIRT1-dependent manner in an optic nerve injury model.

Biochim Biophys Acta Mol Basis Dis. 2024-4

[3]
Healthcare-Seeking Delays in Acute Ischemic Stroke Patients: The Influence of Gender, Immigrant Status, and Educational Background.

Risk Manag Healthc Policy. 2024-1-18

[4]
Melatonin: a modulator in metabolic rewiring in T-cell malignancies.

Front Oncol. 2024-1-8

[5]
Enhancing Sleep Quality: Assessing the Efficacy of a Fixed Combination of Linden, Hawthorn, Vitamin B1, and Melatonin.

Med Sci (Basel). 2023-12-28

[6]
Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism.

Eur J Med Res. 2024-1-20

[7]
The role of the SIRT1-BMAL1 pathway in regulating oxidative stress in the early development of ischaemic stroke.

Sci Rep. 2024-1-20

[8]
Vialinin A alleviates oxidative stress and neuronal injuries after ischaemic stroke by accelerating Keap1 degradation through inhibiting USP4-mediated deubiquitination.

Phytomedicine. 2024-2

[9]
Development of Pharmacological Strategies with Therapeutic Potential in Ischemic Stroke.

Antioxidants (Basel). 2023-12-12

[10]
Oxidative Stress and Antioxidant Defense Mechanisms in Acute Ischemic Stroke Patients with Concurrent COVID-19 Infection.

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