MRI of cerebral oedema in ischaemic stroke and its current use in routine clinical practice DOI Creative Commons
Jakub Čivrný, Tomáš Dorňák, Marie Černá

и другие.

Neuroradiology, Год журнала: 2023, Номер 66(3), С. 305 - 315

Опубликована: Дек. 16, 2023

Abstract Currently, with the knowledge of role collateral circulation in development cerebral ischaemia, traditional therapeutic windows are being prolonged, time not only criterion. Instead, a more personalised approach is applied to select additional patients who might benefit from active treatment. This review briefly describes current pathophysiology early ischaemic changes, capabilities MRI depict such and basics routinely used imaging techniques broadly available for assessment individual phases summarises possible clinical use routine MR imaging, including patient selection treatment outcome on basis imaging.

Язык: Английский

Dystrophin 71 deficiency causes impaired aquaporin-4 polarization contributing to glymphatic dysfunction and brain edema in cerebral ischemia DOI Creative Commons
Jian Yang, Chang Cao, Jiale Liu

и другие.

Neurobiology of Disease, Год журнала: 2024, Номер 199, С. 106586 - 106586

Опубликована: Июнь 29, 2024

Язык: Английский

Процитировано

6

Post-Ischemic Permeability of the Blood–Brain Barrier to Amyloid and Platelets as a Factor in the Maturation of Alzheimer’s Disease-Type Brain Neurodegeneration DOI Open Access
Ryszard Pluta, Barbara Miziak, Stanisław J. Czuczwar

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(13), С. 10739 - 10739

Опубликована: Июнь 27, 2023

The aim of this review is to present evidence the impact ischemic changes in blood–brain barrier on maturation post-ischemic brain neurodegeneration with features Alzheimer’s disease. Understanding processes involved permeability during recirculation will provide clinically relevant knowledge regarding neuropathological that ultimately lead dementia disease type. In review, we try distinguish between primary and secondary after ischemia. Therefore, can observe two hit stages contribute development. onset pathology includes neuronal damage death followed by injury serum leakage amyloid into tissue, leading increased susceptibility neurotoxicity, culminating formation plaques ending full-blown

Язык: Английский

Процитировано

13

Targeted ablation of signal transducer and activator of transduction 1 alleviates inflammation by microglia/macrophages and promotes long-term recovery after ischemic stroke DOI Creative Commons
Wenxuan Han, Hongjian Pu, Sicheng Li

и другие.

Journal of Neuroinflammation, Год журнала: 2023, Номер 20(1)

Опубликована: Июль 29, 2023

Abstract Background Brain microglia and macrophages (Mi/MΦ) can shift to a harmful or advantageous phenotype following an ischemic stroke. Identification of key molecules that regulate the transformation resting Mi/MΦ could aid in development innovative therapies for The transcription factor signal transducer activator transduction 1 (STAT1) has been found contribute acute neuronal death (in first 24 h) stroke, but its effects on influence long-term stroke outcomes have yet be determined. Methods We generated mice with tamoxifen-induced, Mi/MΦ-specific knockout (mKO) STAT1 driven by Cx3cr1 CreER . Expression was examined brain flow cytometry RNA sequencing after induced transient middle cerebral artery occlusion (MCAO). impact mKO cell death, phenotype, inflammation profiles were 3–5 days MCAO. Neurological deficits integrity gray white matter assessed 5 weeks MCAO various neurobehavioral tests immunohistochemistry. Results activated at subacute stage (3 days) Selective deletion did not alter infarct size h MCAO, attenuated release high mobility group box increased arginase 1-producing 3d suggesting boosted inflammation-resolving responses Mi/MΦ. As result, had mitigated less injury long term. Importantly, sufficient improve functional recovery least both male female mice. Conclusions Mi/MΦ-targeted KO does provide immediate neuroprotection augments actions Mi/MΦ, thereby facilitating is, therefore, promising therapeutic target harness beneficial

Язык: Английский

Процитировано

11

Targeted Delivery of Macrophage Membrane Biomimetic Liposomes Through Intranasal Administration for Treatment of Ischemic Stroke DOI Creative Commons
Tianshu Liu, Mengfan Zhang, Jin Z. Zhang

и другие.

International Journal of Nanomedicine, Год журнала: 2024, Номер Volume 19, С. 6177 - 6199

Опубликована: Июнь 1, 2024

Purpose: Ginsenoside Rg3 (Rg3) and Panax notoginseng saponins (PNS) can be used for ischemic stroke treatment, however, the lack of targeting to region limits therapeutic effect. To address this, we leveraged affinity macrophage membrane proteins inflamed brain microvascular endothelial cells develop a membrane-cloaked liposome loaded with PNS (MM-Lip-Rg3/PNS), which precisely target lesion through intranasal administration. Methods: MM-Lip-Rg3/PNS was prepared by co-extrusion method performed characterization, stability, surface protein, morphology. The cellular uptake, immune escape ability, blood-brain barrier crossing ability were studied in vitro. vivo targeting, biodistribution anti-ischemic efficacy evaluated MACO rats, determined diversity nasal pathway olfactory nerve blockade model rats. Finally, pharmacokinetics index investigated. Results: Our results indicated that spherical shell-core structure. avoid mononuclear phagocytosis, actively bind inflammatory cells, have cross barrier. Moreover, could specifically sites, even microglia, increase cumulative number drugs brain, improve environment reduce infarct size. By comparing nerve-blocking rats normal it found there are direct indirect pathways entry into brain. Pharmacokinetics demonstrated exhibited stronger prolonged drug half-life. Conclusion: might contribute accumulation area treatment efficacy. This biomimetic nano-drug delivery system provides new promising strategy stroke. Keywords: macrophage-membrane coating, liposome, stroke,

Язык: Английский

Процитировано

4

The cornel Iridoid glycoside attenuated brain edema of the cerebral ischemia/reperfusion rats by modulating the polarized aquaporin 4 DOI Creative Commons
Zhaoyang Wang,

Fangli Xue,

Jianmei Zhang

и другие.

Fitoterapia, Год журнала: 2024, Номер 177, С. 106098 - 106098

Опубликована: Июнь 29, 2024

Brain edema after ischemic stroke could worsen cerebral injury in patients who received intravenous thrombolysis. Cornus officinalis Sieb. et Zucc., a long-established traditional Chinese medicine, is beneficial to the treatment of neurodegenerative diseases including stroke. In particular, its major component, cornel iridoid glycoside (CIG), was evidenced exhibit neuroprotective effects against ischemic/reperfusion (CIR/I). Aimed explore CIG on brain CIR/I rats, analyzed with main constituents by using HPLC. The molecular docking analysis performed between and AQP4-M23. TGN-020, an AQP4 inhibitor, used as comparison. vivo experiments, rats were pre-treated injured performing middle artery occlusion/reperfusion (MCAO/R). After 24 h, examined for neurological function, pathological changes, edema, polarized Aqp4 expressions brain. HPLC indicated that composed morroniside loganin. showed both loganin displayed lower binding energies AQP4-M23 than TGN-020. exhibited fewer function deficits, minimized swelling, reduced lesion volumes compared MCAO/R rats. peri-infarct infarct regions, pre-treatment restored expression which lost results suggested attenuate ischemia/reperfusion modulating through interaction

Язык: Английский

Процитировано

4

Exosomes: the next-generation therapeutic platform for ischemic stroke DOI Creative Commons
Wenjing Yin,

Hongyin Ma,

Qu Yang

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(5), С. 1221 - 1235

Опубликована: Май 10, 2024

Current therapeutic strategies for ischemic stroke fall short of the desired objective neurological functional recovery. Therefore, there is an urgent need to develop new methods treatment this condition. Exosomes are natural cell-derived vesicles that mediate signal transduction between cells under physiological and pathological conditions. They have low immunogenicity, good stability, high delivery efficiency, ability cross blood-brain barrier. These properties exosomes potential lead breakthroughs in stroke. The rapid development nanotechnology has advanced application engineered exosomes, which can effectively improve targeting ability, enhance efficacy, minimize dosages needed. Advances technology also driven clinical translational research on exosomes. In review, we describe effects their positive roles current stroke, including anti-inflammation, anti-apoptosis, autophagy-regulation, angiogenesis, neurogenesis, glial scar formation reduction effects. However, it worth noting that, despite significant potential, remains a dearth standardized characterization efficient isolation techniques capable producing highly purified Future optimization should prioritize exploration suitable establishment unified workflows harness diagnostic or applications Ultimately, our review aims summarize understanding exosome-based prospects foster innovative ideas therapies.

Язык: Английский

Процитировано

3

Neuroprotective Effects, Mechanisms of Action and Therapeutic Potential of the Kv7/KCNQ Channel Opener QO-83 in Ischemic Stroke DOI
Huiran Zhang,

Yanfei Tian,

Yan Zhang

и другие.

Translational Stroke Research, Год журнала: 2025, Номер unknown

Опубликована: Янв. 24, 2025

Язык: Английский

Процитировано

0

The Mechanism of Bovis Culus Sativus Protecting BBB Damage in Stroke: Insights from Network Pharmacology, Bioinformatics, and Experiments DOI
Mihong Ren, Yong Li, Jianmei Yuan

и другие.

Journal of Ethnopharmacology, Год журнала: 2025, Номер unknown, С. 119390 - 119390

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Neuroprotective effects of hirudin against cerebral ischemia-reperfusion injury via inhibition of CCL2-mediated ferroptosis and inflammatory pathways DOI Creative Commons
J. Y. Liao,

Huahui Chen,

Yiwei Liao

и другие.

Brain Research Bulletin, Год журнала: 2025, Номер unknown, С. 111293 - 111293

Опубликована: Март 1, 2025

Cerebral ischemia-reperfusion injury (CIRI) is a leading cause of neurological impairment in stroke, primarily correlated to oxidative stress, inflammation, and ferroptosis. This study investigates the neuroprotective effects hirudin on CIRI, focusing its role modulating neuronal survival, ferroptosis markers through inhibition CCL2. A middle cerebral artery occlusion (MCAO) model mice an oxygen-glucose deprivation/reoxygenation (OGD/R) HT22 cells were used simulate ischemic conditions. Hirudin significantly improved function reduced edema infarct size MCAO model. In vitro, enhanced viability apoptosis OGD/R-stimulated cells. Integrative network pharmacology transcriptomic analysis identified CCL2 as potential target hirudin. treatment suppressed expression, which turn TLR4/NF-κB signaling activation, thereby mitigating inflammatory responses neurons. Overexpression partially reversed these protective effects, underscoring injury. These findings suggest that alleviates CIRI by preventing ferroptosis, offering insights into therapeutic agent for

Язык: Английский

Процитировано

0

LRRC8A in endothelial cells contributes to the aberrant blood-brain barrier integrity in ischaemic stroke DOI Creative Commons

Yanfei Tian,

Yan Wang,

Yupeng Zhao

и другие.

Stroke and Vascular Neurology, Год журнала: 2025, Номер unknown, С. svn - 003675

Опубликована: Март 16, 2025

Background The increased permeability of the blood-brain barrier (BBB) is a critical contributor to high mortality following ischaemic stroke. However, mechanisms regulating BBB integrity remain poorly understood. Leucine-rich repeat-containing 8A (LRRC8A) chloride channel for cellular volume homeostasis and plays key role in neuronal injury during ischaemia. its impact on function currently unclear. Methods A transient middle cerebral artery occlusion model was established investigate LRRC8A integrity. Laser speckle contrast imaging used monitor cortical blood flow. Primary mouse human brain microvascular endothelial cells (m/hBMVECs) were subjected oxygen-glucose deprivation (OGD) re-oxygenation varying durations. Patch-clamp recordings performed measure volume-regulated currents. Immunostaining conducted evaluate protein expression. Cell evaluated with transwell assay. Results deletion ameliorates infarct area mitigates leakage. Ischaemia dramatically upregulates expression cells, concurrently downregulating tight junction proteins. OGD exposure augments VRCC current mediated by BMVECs. In contrast, inhibiting promotes ZO-1 VE-cadherin, thereby preserving cells. With-no-lysine kinase 1 (WNK1) inhibition contributes LRRC8A-induced damage post-ischaemic Eupatorin, newly identified inhibitor, exerts neuroprotective effects against Conclusions BMVECs pivotal modulating integrity, process regulated WNK1. As an Eupatorin holds potential stroke therapy.

Язык: Английский

Процитировано

0