miRNA Involvement in Cerebral Ischemia-Reperfusion Injury DOI Creative Commons
Maria Adriana Neag, Andrei-Otto Mitre, Codrin-Constantin Burlacu

et al.

Frontiers in Neuroscience, Journal Year: 2022, Volume and Issue: 16

Published: June 10, 2022

Cerebral ischemia reperfusion injury is a debilitating medical condition, currently with only limited amount of therapies aimed at protecting the cerebral parenchyma. Micro RNAs (miRNAs) are small, non-coding RNA molecules that via RNA-induced silencing complex either degrade or prevent target messenger from being translated and thus, can modulate synthesis proteins. In neurological field, miRNAs have been evaluated as potential regulators in brain development processes pathological events. Following ischemic hypoxic stress, cellular molecular events initiated dysregulate different miRNAs, responsible for long-terming progression extension neuronal damage. Because their ability to regulate proteins, emerge possible therapeutic strategy limiting damage following event. This review aims summarize recent literature evidence involved signaling modulating ischemia-reperfusion injuries, thus pointing repair mechanisms. An in-depth overview pathways involvement specific could provide future perspectives neuroprotective agents targeting these miRNAs.

Language: Английский

Network pharmacology, a promising approach to reveal the pharmacology mechanism of Chinese medicine formula DOI
Li Zhao, Hong Zhang, Ning Li

et al.

Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 309, P. 116306 - 116306

Published: Feb. 27, 2023

Language: Английский

Citations

418
Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke DOI
Diana Alsbrook, Mario Di Napoli, Kunal Bhatia

et al.

Current Neurology and Neuroscience Reports, Journal Year: 2023, Volume and Issue: 23(8), P. 407 - 431

Published: July 3, 2023

Language: Английский

Citations

145
Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects DOI Open Access

Zhengming Tian,

Xunming Ji, Jia Liu

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(11), P. 6224 - 6224

Published: June 2, 2022

Vascular cognitive impairment and dementia (VCID) is a major heterogeneous brain disease caused by multiple factors, it the second most common type of in world. It long-term chronic low perfusion whole or local area, eventually develops into severe dysfunction syndrome. Because disease's ambiguous classification diagnostic criteria, there no clear treatment strategy for VCID, association between cerebrovascular pathology controversial. Neuroinflammation an immunological cascade reaction mediated glial cells central nervous system where innate immunity resides. Inflammatory reactions could be triggered various damaging events, including hypoxia, ischemia, infection. Long-term hypoperfusion-induced ischemia hypoxia can overactivate neuroinflammation, causing apoptosis, blood-brain barrier damage other pathological changes, triggering aggravating occurrence development VCID. In this review, we will explore mechanisms neuroinflammation induced hypoperfusion emphasize important role VCID from perspective immune cells, mediators signaling pathways, so as to provide valuable ideas prevention disease.

Language: Английский

Citations

103
Oxidative Stress in Ischemia/Reperfusion Injuries following Acute Ischemic Stroke DOI Creative Commons
Anamaria Jurcău, Adriana Ioana Ardelean

Biomedicines, Journal Year: 2022, Volume and Issue: 10(3), P. 574 - 574

Published: March 1, 2022

Recanalization therapy is increasingly used in the treatment of acute ischemic stroke. However, about one third these patients, recanalization followed by ischemia/reperfusion injuries, and clinically to worsening neurological status. Much research has focused on unraveling involved mechanisms order prevent or efficiently treat injuries. What we know so far that oxidative stress mitochondrial dysfunction are significantly pathogenesis injury. despite promising results obtained experimental research, clinical studies trying interfere with pathways have mostly failed. The current article discusses main leading such as dysfunction, excitotoxicity, stress, reviews trials antioxidant molecules highlighting recent developments future strategies.

Language: Английский

Citations

94
Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer’s Disease Progression DOI Open Access
Felicia Liana Andronie-Cioară, Adriana Ioana Ardelean, Carmen Delia Nistor-Cseppento

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(3), P. 1869 - 1869

Published: Jan. 18, 2023

Aging is the most prominent risk factor for late-onset Alzheimer’s disease. associates with a chronic inflammatory state both in periphery and central nervous system, evidence thereof mechanisms leading to neuroinflammation being discussed. Nonetheless, significantly enhanced by accumulation of amyloid beta accelerates progression disease through various pathways discussed present review. Decades clinical trials targeting 2 abnormal proteins disease, tau, led many failures. As such, via different strategies could prove valuable therapeutic strategy, although much research still needed identify appropriate time window. Active focusing on identifying early biomarkers help translating these novel from bench bedside.

Language: Английский

Citations

84
The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms DOI Open Access
Ming‐Chang Chiang, Tsung‐Yu Tsai,

Chieh-Ju Wang

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(7), P. 6328 - 6328

Published: March 28, 2023

Neuroinflammation is a critical factor in developing and progressing numerous brain diseases, including neurodegenerative diseases. Chronic or excessive neuroinflammation can lead to neurotoxicity, causing damage contributing the onset progression of various Therefore, understanding mechanisms strategies control them crucial for treating Studies have shown that plays vital role such as Alzheimer's (AD) Parkinson's (PD), stroke. Additionally, effects PM

Language: Английский

Citations

84
Quercetin improves cerebral ischemia/reperfusion injury by promoting microglia/macrophages M2 polarization via regulating PI3K/Akt/NF-κB signaling pathway DOI Open Access
Lin Li, Weifeng Jiang,

Baojian Yu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 168, P. 115653 - 115653

Published: Oct. 7, 2023

The modulation of microglial polarization from the pro-inflammatory M1 to anti-inflammatory M2 phenotype shows promise as a therapeutic strategy for ischemic stroke. Quercetin, natural flavonoid abundant in various plants, possesses anti-inflammatory, anti-apoptotic, and antioxidant properties. Nevertheless, its effect underlying mechanism on microglia/macrophages M1/M2 treatment cerebral ischemia/reperfusion injury (CI/RI) remain poorly explored. In current study, we observed that quercetin ameliorated neurological deficits, reduced infarct volume, decreased number (CD16/32+/Iba1+), enhanced (CD206+/Iba1+) after establishing CI/RI model rats. Subsequent vivo vitro experiments indicated downregulated markers (CD86, iNOS, TNF-α, IL-1β, IL-6) upregulated (CD206, Arg-1, IL-10, TGF-β). Network pharmacology analysis molecular docking revealed PI3K/Akt/NF-κB signaling pathway emerged core pathway. Western blot confirmed phosphorylation PI3K Akt, while alleviating IκBα NF-κB both vitro. However, inhibitor LY294002 reversed effects expression key proteins primary microglia oxygen-glucose deprivation/reoxygenation (OGD/R) Collectively, our findings demonstrate facilitates by modulating CI/RI. These provide novel insights into mechanisms

Language: Английский

Citations

79
Selenium Alleviates Cerebral Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Fusion and Ferroptosis DOI Creative Commons
Yuanyuan Shi, Lijian Han, Xianxian Zhang

et al.

Neurochemical Research, Journal Year: 2022, Volume and Issue: 47(10), P. 2992 - 3002

Published: June 20, 2022

To clarify the potential role of selenium (Se) on cerebral ischemia/reperfusion (I/R) injury, we utilized mouse middle artery occlusion (MCAO) followed by reperfusion as an animal model and oxygen-glucose deprivation reoxygenation (OGD/R) to treat N2a cells a cell model, respectively. MCAO was established in mice then divided into different groups with or without Se treatment. TTC staining used observe whether I/R modeling successful, apoptosis level determined TUNEL staining. The expression GPx-4 p22phox assessed western blot. In vitro experiments, OGD/R induced oxidative stress levels GSH/GSSG, malondialdehyde, superoxide dismutase iron content, QRT-PCR detect mRNA Cox-2, Fth1, Mfn1 mtDNA cells. JC-1 flow cytometry performed mitochondrial membrane potential. treatment alleviated injury improved survival rate mice. Additionally, apparently attenuated inhibited accumulation terms its mechanism, could up-regulate alleviate ferroptosis promoting fusion vivo vitro. These findings suggest that may have great alleviating injury.

Language: Английский

Citations

74
Neutrophil Targeting Platform Reduces Neutrophil Extracellular Traps for Improved Traumatic Brain Injury and Stroke Theranostics DOI Creative Commons
Qingchun Mu, Kai Yao, Madiha Zahra Syeda

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: 11(21)

Published: March 23, 2024

Abstract Traumatic brain injuries (TBI) and stroke are major causes of morbidity mortality in both developing developed countries. The complex heterogeneous pathophysiology TBI cerebral ischemia‐reperfusion injury (CIRI), addition to the blood‐brain barrier (BBB) resistance, is a advancement diagnostics therapeutics. Clinical data showed that severity positively correlated with number neutrophils peripheral blood sites. Furthermore, neutrophil extracellular traps (NETs) released by correlate worse outcomes impairing revascularization vascular remodeling. Therefore, targeting deliver NETs inhibitors sites reduce formation can be an optimal strategy for therapy. Herein, study designs synthesizes reactive oxygen species (ROS)‐responsive neutrophil‐targeting delivery system loaded peptidyl arginine deiminase 4 (PAD4) inhibitor, GSK484, prevent sites, which significantly inhibited neuroinflammation improved neurological deficits, survival rate CIRI. This may provide groundwork development targeted theranostics stroke.

Language: Английский

Citations

24
HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation DOI Creative Commons
Jiamin Li, Zixin Wang, Jiameng Li

et al.

Translational Stroke Research, Journal Year: 2024, Volume and Issue: unknown

Published: May 14, 2024

Abstract Stroke in China is distinguished by its high rates of morbidity, recurrence, disability, and mortality. The ultra-early administration rtPA essential for restoring perfusion acute ischemic stroke, though it concurrently elevates the risk hemorrhagic transformation. High-mobility group box 1 (HMGB1) emerges as a pivotal player neuroinflammation after brain ischemia ischemia–reperfusion. Released passively necrotic cells actively secreted, including direct secretion HMGB1 into extracellular space packaging intracellular vesicles immune cells, glial platelets, endothelial represents prototypical damage-associated molecular pattern (DAMP). It intricately involved pathogenesis atherosclerosis, thromboembolism, detrimental inflammation during early phases stroke. Moreover, significantly contributes to neurovascular remodeling functional recovery later stages. Significantly, mediates transformation facilitating neuroinflammation, directly compromising integrity blood–brain barrier, enhancing MMP9 through interaction with rtPA. As systemic inflammatory factor, also implicated post-stroke depression an elevated stroke-associated pneumonia. role extends influencing polarizing various subtypes cells. This includes mediating excitotoxicity due excitatory amino acids, autophagy, release, NET formation, autocrine trophic pathways. Given multifaceted role, recognized crucial therapeutic target prognostic marker stroke In this review, we summarize structure redox properties, pathways, regulation cell activity, pathophysiological mechanisms hemorrhage HMGB1, which will pave way developing new neuroprotective drugs, reduction expansion thrombolysis time window.

Language: Английский

Citations

17