Oxidative Stress in Cerebral Ischemia/Reperfusion Injury DOI Open Access

Roberto Anaya-Fernández,

Roberto Anaya‐Prado,

Michelle M. Anaya-Fernandez

et al.

OBM Neurobiology, Journal Year: 2024, Volume and Issue: 08(03), P. 1 - 15

Published: Aug. 7, 2024

Oxidative stress in cerebral ischemia/reperfusion injury (CIRI) involves reactive oxygen and nitrogen species (ROS RNS). Despite efficient antioxidant pathways the brain, hypoxia triggers production of free radicals downregulates ATP, which leads to oxidative stress. Sources during CIRI include Ca<sup>2+</sup>-dependent enzymes, phospholipid degradation mitochondrial enlargement. Upon reperfusion, abrupt increase a massive radical via enzymes like xantin oxidase (XO), phospholipase A2 (PLA2) oxide synthases (OS). These play an essential role neuronal damage by excitotoxicity, lipoperoxidation, nitrosylation, inflammation programmed cell death (PCD). Endothelial nitric synthase (eNOS) decreases as compared (nNOS). This is associated with damage, endothelial inflammation, apoptosis Strategies promoting activation eNOS while inhibiting nNOS could offer neuroprotective benefits CIRI. Understanding targeting these mitigate brain events. Clinically, tissue plasminogen activator (t-PA) has been shown restore blood flow. However, serious side effects have described, including hemorrhagic transformation. Different treatments are currently under investigation avoid I/R injury. Baicalin reported potential agent that improve t-PA adverse effects, do peroxynitrite synthesis matrix metalloproteinase (MMP) expression. In this review, interventions addressed. Special attention paid mechanisms radicals, especially nNOS-derived (NO). The primary purpose describe accessible activity leading membrane phospholipids breakdown. <strong>Key</strong><strong>w</strong><strong>ords</strong>Oxidative stress; ischemia/reperfusion; oxide; species;

Language: Английский

Naotaifang formula regulates Drp1-induced remodeling of mitochondrial dynamics following cerebral ischemia-reperfusion injury DOI
Ruining She, Heyan Tian,

Feiyue Sun

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

4
The mechanosensitive Piezo1 channel exacerbates myocardial ischaemia/reperfusion injury by activating caspase-8-mediated PANoptosis DOI

Pang‐Bo Li,

Jun-Qin Bai,

Wenxi Jiang

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 139, P. 112664 - 112664

Published: July 14, 2024

Language: Английский

Citations

17
18β-Glycyrrhetinic acid protects against deoxynivalenol-induced liver injury via modulating ferritinophagy and mitochondrial quality control DOI
Junze Jiang,

Xintong Zhou,

Hao Chen

et al.

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134319 - 134319

Published: April 21, 2024

Language: Английский

Citations

14
ZBP1-mediated PANoptosis: A possible novel mechanism underlying the therapeutic effects of penehyclidine hydrochloride on myocardial ischemia–reperfusion injury DOI
Boqun Cui, Zeyou Qi, Wenjun Liu

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 137, P. 112373 - 112373

Published: June 12, 2024

Language: Английский

Citations

13
Analysis of the role of PANoptosis in seizures via integrated bioinformatics analysis and experimental validation DOI Creative Commons
Yueying Liu,

Yuanjin Chang,

Xiaofan Jiang

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(4), P. e26219 - e26219

Published: Feb. 1, 2024

BackgroundEpilepsy is recognized as the most common chronic neurological condition among children, and hippocampal neuronal cell death has been identified a crucial factor in pathophysiological processes underlying seizures. In recent studies, PANoptosis, newly characterized form of death, emerged significant contributor to development various disorders, including Alzheimer's disease, Parkinson's amyotrophic lateral sclerosis. PANoptosis involves simultaneous activation pyroptosis, apoptosis, necroptosis within same population cells. However, its specific role context seizures remains be fully elucidated. Further investigation required uncover precise involvement pathogenesis better understand potential implications for targeted therapeutic approaches epilepsy.MethodsIn this study, gene expression data hippocampus following administration kainic acid (KA) or NaCl was obtained from Gene Expression Omnibus (GEO) database. The PANoptosis-related set compiled GeneCards database previous literature. Time series analysis performed analyze temporal patterns genes. variation (GSVA), ontology (GO), Kyoto encyclopedia genes genomes (KEGG) were employed explore biological mechanisms Weighted co-expression network (WGCNA) differential utilized identify pivotal modules associated with To validate genes, Western blotting quantitative real-time polymerase chain reaction (qRT-PCR) assays conducted. These experimental validations human blood samples, animal models, models verify their relevance epilepsy.ResultsThe GSVA study demonstrated that have distinguish between control group KA-induced epileptic mice. This suggests these are significantly altered response epilepsy. Furthermore, blue module being highly phenotypes. consists exhibit correlated specifically related Within module, 10 further biomarker include MLKL, IRF1, RIPK1, GSDMD, CASP1, CASP8, ZBP1, CASP6, PYCARD, IL18. likely play critical roles pathophysiology epilepsy could serve biomarkers diagnosing monitoring condition.ConclusionIn conclusion, our may closely novel which provides insights into helps

Language: Английский

Citations

9
Chrysin inhibits ferroptosis of cerebral ischemia/reperfusion injury via regulating HIF-1α/CP loop DOI Creative Commons
Jinfeng Shang,

Jiakang Jiao,

Jingyi Wang

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 174, P. 116500 - 116500

Published: March 30, 2024

Chrysin is a natural flavonoid with powerful neuroprotective capacity. Cerebral ischemia/reperfusion injury (CIRI) associated oxidative stress and ferroptosis. Hypoxia-inducible factor 1α (HIF-1α) ceruloplasmin (CP) are the critical targets for oxidation reactions iron transport. But regulatory mechanism between them still unclear. Transient middle cerebral artery occlusion (tMCAO) model in rats oxygen glucose deprivation/re-oxygenation (OGD/R) PC12 cells were applied. Pathological tissue staining biochemical kit used to evaluate effect of chrysin. The relationship HIF-1α CP was verified by transcriptomics, qRT-PCR Western blot. In CIRI, HIF-1α/CP loop discovered be pathway CIRI led activation nuclear translocation HIF-1α, which promoted transcription translation, downstream Inhibition had opposite on ferroptosis regulation. Overexpression increased expression nevertheless, inhibited alleviated CIRI. Silencing elevation nucleus aggravated Mechanistically, chrysin restrained translocation, thereby inhibiting turn reduced mitigated Our results highlight restrains through loop.

Language: Английский

Citations

8
Zinc ions regulate mitochondrial quality control in neurons under oxidative stress and reduce PANoptosis in spinal cord injury models via the Lgals3-Bax pathway DOI

Mingyu Bai,

Yang Cui,

Zelin Sang

et al.

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: 221, P. 169 - 180

Published: May 21, 2024

Language: Английский

Citations

8
Esculentoside H reduces the PANoptosis and protects the blood-brain barrier after cerebral ischemia/reperfusion through the TLE1/PI3K/AKT signaling pathway DOI
Kuo Zhang, Zhichao Wang,

Hongxue Sun

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 379, P. 114850 - 114850

Published: June 12, 2024

Language: Английский

Citations

8
Sufentanil-induced Nrf2 protein ameliorates cerebral ischemia-reperfusion injury through suppressing neural ferroptosis DOI
Xuelian Zhu,

Xi Han,

Jingtao Wang

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 279, P. 135109 - 135109

Published: Aug. 27, 2024

Language: Английский

Citations

8
Ozone-mediated cerebral protection: Unraveling the mechanism through ferroptosis and the NRF2/SLC7A11/GPX4 signaling pathway DOI Creative Commons

Farong Zhu,

Shengyang Ding, Yu Liu

et al.

Journal of Chemical Neuroanatomy, Journal Year: 2024, Volume and Issue: 136, P. 102387 - 102387

Published: Jan. 3, 2024

The pathogenesis of brain ischemic/reperfusion (I/R) insult is characterized by neuronal loss due to excessive oxidative stress responses. Ferroptosis, a form cell death, can be triggered when the balance between antioxidants and pro-oxidants in cells disrupted. Ozone, natural bioactive molecule with antioxidant/anti-apoptotic pro-autophagic properties, has been shown enhance antioxidant system's capacity ameliorate stress. However, its role ferroptosis remains unclear. Therefore, we investigated functions possible mechanisms ozone cerebral I/R-induced ferroptotic death. A ischemia-reperfusion injury model was induced Sprague-Dawley (SD) rats pre-treated ozone. Intraperitoneal administration NRF2 inhibitor ML385, SLC7A11 Erastin, GPX4 RSL3 performed one hour prior establishment. Our results showed that preconditioning mitigated damage caused I/R, reduced severity neurological deficits, lowered infarct volume middle artery occlusion (MCAO) rats, decreased infarcts. Transmission electron microscopy, immunofluorescence, Western blotting indicated following MCAO-induced damage. MCAO resulted morphological mitochondria, increased lipid peroxidation accumulation, elevated malondialdehyde (MDA) production. Furthermore, levels FTH1 (negative regulators ferroptosis) ACSL4 (a positive regulator ferroptosis). Ozone demonstrated neuroprotective effect increasing nuclear translocation expression GPX4. Treatment significantly reversed preconditioning's protective on ferroptosis. findings treatment attenuates ischemia/reperfusion rat via NRF2/SLC7A11/GPX4 pathway, providing theoretical basis for ozone's potential use as therapy prevent ischemic stroke.

Language: Английский

Citations

7