Neurological Sciences, Год журнала: 2023, Номер 44(8), С. 2699 - 2713
Опубликована: Апрель 3, 2023
Язык: Английский
Antioxidants, Год журнала: 2022, Номер 11(12), С. 2377 - 2377
Опубликована: Ноя. 30, 2022
Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral stroke, and recovery blood circulation will lead ischemia-reperfusion injury (CIRI). involves many pathological processes such as oxidative stress, inflammation, mitochondrial dysfunction. Nuclear factor erythroid 2-related 2 (Nrf2), one most critical antioxidant transcription factors cells, can coordinate various cytoprotective inhibit stress. Targeting Nrf2 considered potential strategy prevent treat injury. During ischemia, participates signaling pathways Keap1, PI3K/AKT, MAPK, NF-κB, HO-1, then alleviates or CIRI inhibiting anti-inflammation, maintaining homeostasis, protecting blood–brain barrier, ferroptosis. In this review, we have discussed structure Nrf2, mechanisms related research on treatment through pathway recent years, expounded important role future stroke.
Язык: Английский
Процитировано
182
International Immunopharmacology, Год журнала: 2023, Номер 118, С. 110047 - 110047
Опубликована: Март 28, 2023
Our previous studies have shown that berberine can improve the nerve function deficits in ischemic stroke by inhibiting inflammation. The cellular communication between astrocytes and neurons via exosomes might affect neurological after stroke, which plays a vital role therapy of stroke.The present study focused on effects released from induced glucose oxygen deprivation model with pretreatment (BBR-exos) treatment for its regulatory mechanism.Oxygen-glucose-deprivation/Reoxygenation (OGD/R)-treated primary cells were used to mimic cerebral ischemia/reperfusion conditions vitro. With BBR-exos (OGD/R-exos), cell viability was detected. C57BL/6J mice establish middle artery occlusion/reperfusion (MCAO/R) model. anti-neuroinflammation OGD/R-exos evaluated. Subsequently, key miRNA identified exosomal sequencing validation. miR-182-5p inhibitors provided verify Finally, binding sites Rac1 predicted online verified using dual-luciferase reporter assay.BBR-exos both improved decreased activity OGD/R-induced neurons, expression IL-1β, IL-6 TNF-α (all P ＜ 0.05), reduced neuronal injury inhibited neuroinflammation Vitro. And showed better (P 0.05). same effect has been vivo experiments: MCAO/R Likewise, results highly expressed targeting 0.05).BBR-exos carry injured inhibit Rac1, could brain stroke.
Язык: Английский
Процитировано
33
European Journal of Pharmacology, Год журнала: 2023, Номер 953, С. 175860 - 175860
Опубликована: Июнь 16, 2023
Язык: Английский
Процитировано
26
Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)
Опубликована: Янв. 29, 2024
Microglia is the major contributor of post-stroke neuroinflammation cascade and crucial cellular target for treatment ischemic stroke. Currently, endogenous mechanism underlying microglial activation following stroke remains elusive. Serglycin (SRGN) a proteoglycan expressed in immune cells. Up to now, role SRGN on largely unexplored.
Язык: Английский
Процитировано
18
CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(3)
Опубликована: Март 1, 2024
Abstract Objectives FTO is known to be involved in cerebral ischemia/reperfusion (I/R) injury. However, its related specific mechanisms during this condition warrant further investigations. This study aimed at exploring the impacts of and FYN/DRP1 axis on mitochondrial fission, oxidative stress (OS), ferroptosis I/R injury underlying mechanisms. Methods The models were established mice via temporary middle artery occlusion/reperfusion (tMCAO/R) hypoxia/reoxygenation induced mouse hippocampal neurons oxygen–glucose deprivation/reoxygenation (OGD/R). After gain‐ loss‐of‐function assays, gene expression was detected, along with examination OS‐ ferroptosis‐related marker levels, neuronal degeneration infarction, cell viability apoptosis. binding FYN, m6A modification levels interaction between FYN Drp1 evaluated. Results downregulated upregulated tMCAO/R OGD/R models. overexpression inhibited OS, suppress mice, which reversed by overexpressing FYN. also suppressed fission increase survival inhibit apoptosis models, aggravated additionally inhibiting DRP1. inactive signaling, thus reducing enhancing cells. Conclusions through modification, thereby subduing activity relieving
Язык: Английский
Процитировано
13
Journal of Neuroimmune Pharmacology, Год журнала: 2025, Номер 20(1)
Опубликована: Фев. 3, 2025
Stroke represents a significant burden on global health and the economy, with high mortality rates, disability, recurrence. Ischemic stroke is serious condition that occurs when blood vessel in brain interrupted, reducing supply to affected area. Inflammation component pathophysiology. Neuroinflammation triggered following acute ischemic ictus, where blood–brain barrier (BBB) breaks down, causing damage endothelial cells. The will eventually generate oxidative stress, activate pathological phenotypes of astrocytes microglia, lead neuronal death neurovascular unit. As result, unleashes robust neuroinflammatory response, which can further worsen neurological outcomes. complex process involved repair. Finding new neuroinflammation molecular targets essential develop effective safe novel treatment approaches against stroke. Accumulating studies have investigated pharmacological properties cannabinoids (CBs) for many years, recent research has shown their potential therapeutic use treating rodent models. These findings revealed promising impacts CBs cellular ameliorating deficits. In this review, we explore possibility administration mitigating caused by We summarize results from several preclinical evaluating efficacy anti-inflammatory interventions Although convincing evidence implies targeting are stroke, translating these into clinical setting proven be challenging. translation hurdle due essence ability cause anxiety, cognitive deficit, psychosis. Future warranted address dose-beneficial effect trials stroke-related treatment.
Язык: Английский
Процитировано
2
Neurochemical Research, Год журнала: 2022, Номер 48(3), С. 980 - 995
Опубликована: Ноя. 26, 2022
Язык: Английский
Процитировано
34
Phytomedicine, Год журнала: 2022, Номер 105, С. 154373 - 154373
Опубликована: Авг. 1, 2022
Язык: Английский
Процитировано
32
Current Neurovascular Research, Год журнала: 2023, Номер 20(3), С. 346 - 353
Опубликована: Июнь 26, 2023
Electroacupuncture (EA) treatment has been recommended by World Health Organization (WHO) for years on cerebral ischemia treatment, but the specific mechanism is still elusive. Studies have shown that EA can relieve brain damage after ischemic stroke inhibiting programmed cell death (PCD), such as apoptosis, necroptosis, and autophagy. Ferroptosis, a unique form of death, highlighted recently found to occur in I/R injury. We, therefore, investigated whether plays an essential role relieving injury via ferroptosis.The modified MCAO/R rats model was established then divided into four groups with or without treatment. Neurological deficit score TTC staining were used evaluate neurological infarct volume each group. Transmission electron microscope (TEM) immunofluorescence applied mitochondrial ultrastructure ROS accumulation observation, respectively. The proteins mRNA expression ACSL4, TFR1, GPX4 assessed western blot qPCR detect progress ferroptosis.EA improved deficits reduced volume. Moreover, significantly relieved morphological changes inhibited Production MCAO rats. In terms its mechanism, obviously decreased ACSL4 TFR1 expressions promoted levels rats.These findings indicate might play ferroptosis.
Язык: Английский
Процитировано
19
Neurochemical Research, Год журнала: 2024, Номер 49(7), С. 1806 - 1822
Опубликована: Май 7, 2024
Язык: Английский
Процитировано
8