NOD-like receptor X1 promotes autophagy and inactivates NLR family pyrin domain containing 3 inflammasome signaling by binding autophagy-related gene 5 to alleviate cerebral ischemia/reperfusion-induced neuronal injury.

Ischemic strokes pose serious risks to human health. We aimed to elucidate the function of NOD-like receptor X1 (NLRX1) in a rat middle cerebral artery occlusion (MCAO)-induced cerebral ischemia/reperfusion injury (CIRI) model and in an oxygen-glucose deprivation/reperfusion (OGD/R)-treated human microglial cell line (HMC3) model. Following NLRX1 upregulation, infarct volumes were measured with 2,3,5-triphenyltetrazolium chloride staining and pathological examination was conducted with hematoxylin-eosin staining.

Pathological roles of mitochondrial dysfunction in endothelial cells during the cerebral no-reflow phenomenon: A review.

Emergency intravascular interventional therapy is the most effective approach to rapidly restore blood flow and manage occlusion of major blood vessels during the initial phase of acute ischemic stroke. Nevertheless, several patients continue to experience ineffective reperfusion or cerebral no-reflow phenomenon, that is, hypoperfusion of cerebral blood supply after treatment. This is primarily attributed to downstream microcirculation disturbance.

Flavonoids from as neuroprotective agents attenuate cerebral ischemia/reperfusion injury and via activating Nrf2.

Objectives: Cerebral ischemic stroke is a leading cause of death worldwide. Though timely reperfusion reduces the infarction size, it exacerbates neuronal apoptosis due to oxidative stress. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor regulating the expression of antioxidant enzymes.

Remote ischaemic conditioning for neurological disorders-a systematic review and narrative synthesis.

Introduction: Remote ischaemic conditioning (RIC) refers to the use of controlled transient ischemic and reperfusion cycles, commonly of the upper or lower limb, to mitigate cellular damage from ischaemic injury. Preclinical studies demonstrate that RIC may have a neuroprotective effect and therefore could represent a novel therapeutic option in the management of neurological disorders. The aim of this review is to comprehensively describe the current clinical evidence of RIC in neurological disorders.

Nek6 regulates autophagy through the mTOR signaling pathway to alleviate cerebral ischemia-reperfusion injury.

Objective: Cerebral ischemia-reperfusion injury (CIRI) is a major obstacle to neurological recovery after clinical treatment of ischemic stroke. The aim of this study was to investigate the molecular mechanism of Nek6 alleviating CIRI through autophagy after cerebral ischemia.

Materials And Methods: A mouse model of CIRI was constructed by middle cerebral artery occlusion (MCAO).

Astragalus membranaceus-Carthamus tinctorius herb pair antagonizes parthanatos in cerebral ischemia/reperfusion injury via regulating PARP-1/TAX1BP1-mediated mitochondrial respiratory chain complex I.

Ethnopharmacological Relevance: The combination of Astragalus membranaceus (Huang Qi in Chinese, HQ) and Carthamus tinctorius (Hong Hua in Chinese, HH) is commonly employed for treating ischemic stroke (IS). The heavily oxidative environment of cerebral ischemia/reperfusion injury (CI/RI) promotes activation of poly (ADP-ribose) polymerase-1 (PARP-1), which initiates parthanatos, a regulated cell death mode. Reactive oxygen species (ROS) bursting in mitochondrial respiratory chain complex I (Complex I) is a key cause of CI/RI.

Electroacupuncture inhibits neuronal pyroptosis in ischemic brain injury through modulating SIRT5-mediated NEK7 succinylation.

Ischemic stroke is a leading cause of global death. The treatment of this disease can inevitably result in reperfusion, thereby triggering cerebral ischemia-reperfusion injury (IRI) and neuronal pyroptosis. Electroacupuncture derived from traditional acupuncture has been proven to have favorable effects on ameliorating brain IRI and pyroptosis.

Long non-coding RNA OIP5-AS1 protects neurons from ischemia-reperfusion injury and inhibits neuronal apoptosis through TAB-2.

Ischemic stroke represents a highly perilous cerebrovascular disorder, involving a variety of complex pathophysiological mechanisms. OIP5 antisense RNA 1 (OIP5-AS1) is a long non-coding RNA (LncRNA) that has been shown to play a pivotal role in a variety of disease systems. However, there are relatively few studies on ischemic stroke.

Energy restriction inhibits β-catenin ubiquitination to improve ischemic stroke injury via USP18/SKP2 axis.

Ischemic stroke (IS) remains a global health issue because of its great disability and mortality. Energy restriction (ER) has been justified to perform an inhibitory role in cerebral injury caused by IS. This research was purposed to inquire the potential molecular mechanism of ER in IS.

The Effect of Acute Stroke Treatment on S100B, IMA, and Thiol-Disulfide Balance.

Background: A variety of processes, ranging from blood-brain barrier disruption to circulating biomarkers, contributes to reperfusion injury in acute stroke treatment.

Objective: We aimed to investigate the effects of thrombolytic therapy and endovascular thrombectomy therapy on serum S100 calcium-binding protein B, ischemia-modified albumin and thiol-disulfide balance in patients who arrived within the first 6 h of acute ischemic stroke.

Material And Methods: The study considered 66 patients with the diagnosis of acute ischemic stroke who underwent thrombolytic therapy or EVT in the first 6 h, as well as 32 healthy volunteers.

Assessing the impact of gut microbiota and metabolic products on acute lung injury following intestinal ischemia-reperfusion injury: harmful or helpful?

Ischemia-reperfusion injury (IRI) is a common and clinically significant form of tissue damage encountered in medical practice. This pathological process has been thoroughly investigated across a variety of clinical settings, including, but not limited to, sepsis, organ transplantation, shock, myocardial infarction, cerebral ischemia, and stroke. Intestinal IRI, in particular, is increasingly recognized as a significant clinical entity due to marked changes in the gut microbiota and their metabolic products, often described as the body's "second genome.

The Therapeutic Effects of SP-8356, a Verbenone Derivative, with Multimodal Cytoprotective Mechanisms in an Ischemic Stroke Rat Model.

An ischemic cerebral stroke results from the interruption of blood flow to the brain, triggering rapid and complex cascades of excitotoxicity, oxidative stress, and inflammation. Current reperfusion therapies, including intravenous thrombolysis and mechanical thrombectomy, cause further brain injury due to reperfusion-induced cytotoxicity. To date, novel cytoprotective therapies that could address these challenges have yet to be developed, likely due to the limitations of targeting a single pathologic mechanism.

The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption.

Light alcohol consumption (LAC) may reduce the incidence and improve the prognosis of ischemic stroke. Recently, we found that LAC promotes cerebral angiogenesis and inhibits early inflammation following ischemic stroke. In addition, LAC upregulates lipocalin-type prostaglandin D2 synthase (L-PGDS) in the brain.

Unveiling Smyd-2's Role in Cytoplasmic Nrf-2 Sequestration and Ferroptosis Induction in Hippocampal Neurons After Cerebral Ischemia/Reperfusion.

SET and MYND Domain-Containing 2 (Smyd-2), a specific protein lysine methyltransferase (PKMT), influences both histones and non-histones. Its role in cerebral ischemia/reperfusion (CIR), particularly in ferroptosis-a regulated form of cell death driven by lipid peroxidation-remains poorly understood. This study identifies the expression of Smyd-2 in the brain and investigates its relationship with neuronal programmed cell death (PCD).

VNS facilitates the neurological function recovery after ischemia/reperfusion injury by regulating the A1/A2 polarization of astrocytes through the NMU-NMUR2 pathway.

Stroke is the second leading cause of death worldwide. Although conventional treatments such as thrombolysis and mechanical thrombectomy are effective, their narrow therapeutic window limits long-term neurological recovery. Previous studies have shown that vagus nerve stimulation (VNS) enhances neurological recovery after ischemia/reperfusion (I/R) injury, and neuromedin U (NMU) has neuroprotective effects.

A narrative review of vagus nerve stimulation in stroke.

Stroke is a significant health concern impacting society and the health care system. Reperfusion therapy for acute ischemic stroke and standard rehabilitative therapies may not always be effective at improving post-stroke neurological function, and developing alternative strategies is particularly important. Vagus nerve stimulation (VNS) is a treatment option currently approved by the Food and Drug Administration (FDA) for intractable epilepsy, refractory depression, primary headache disorders, obesity, and moderate to severe upper-limb motor dysfunction in chronic ischemic stroke patients.

Calycosin Ameliorates Neuroinflammation via TLR4-Mediated Signal Following Cerebral Ischemia/Reperfusion Injury in vivo and in vitro.

Background: Cerebral ischemia-reperfusion injury (CIRI) is a key pathophysiological process that leads to stroke mortality, with TLR4-mediated inflammation playing a crucial role. Our previous research highlighted the neuroprotective effects of the phytoestrogen calycosin on CIRI, although the precise mechanism remains unclear. This study aimed to explore the effects of calycosin on the HMGB1/TLR4/NF-κB signaling pathway in rat models of CIRI, both in vivo and in vitro.

Assessment of corticospinal tract damage and cytokines response in early and late stages of acute unilateral brainstem infarction patients.

Background: Acute brainstem infarction is associated with high morbidity and mortality, the integrity of corticospinal tract (CST) detected via diffusion tensor imaging (DTI) can assist in predicting the motor recovery of the patients. In addition to the damage caused by ischemia and reperfusion, sterile inflammation also contributes to the brain injury after stroke. However, the changes in CST integrity detected by DTI in acute brainstem infarction have yet to be fully elucidated, and it is still unclear whether sterile inflammation can cause damage to the CST.

Pinocembrin activation of DPP9 inhibits NLRP1 inflammasome activation to alleviate cerebral ischemia/reperfusion-induced lung and intestinal injury.

After stroke, there is a high incidence of acute lung injury and impairment of intestinal barrier function. In this research, the effects of pinocembrin on organ injuries induced by cerebral ischemia-reperfusion were investigated in mice with middle cerebral artery occlusion/reperfusion (MCAO/R) and further explored the possible mechanism. The potential targets of pinocembrin against MCAO/R were obtained by online tools.

An ultrasonic degraded polysaccharide extracted from Pueraria lobata ameliorate ischemic brain injury in mice by regulating the gut microbiota and LPS-TLR4 pathway.

Ischemia brain injury is closely associated with the gut microbiota. Polysaccharides, as a typical prebiotic, have been extensively employed in stroke treatment. In our previous study, Pueraria lobata polysaccharide (PLP-3) with antioxidant activity was prepared via water extraction and alcohol precipitation combined with ultrasonic degradation.

Lactate modulates microglial inflammatory responses through HIF-1α-mediated CCL7 signaling after cerebral ischemia in mice.

Lactate is a potent regulator of neuroinflammation. We recently demonstrated that lactate alleviated neuronal injury via HIF-1α-regulated microglial inflammation after oxygen-glucose deprivation (OGD). However, the underlying mechanisms and the effect of lactate on microglial responses after ischemic stroke remained unknown.

Tetramethylpyrazine attenuates cerebral ischemia-reperfusion injury by inhibiting ferroptosis via the AMPK / Nrf2 pathways.

Objectives: Ferroptosis is involved in the development and exacerbation of cerebral ischemia-reperfusion injury (CIRI), and its inhibition can alleviate CIRI. Tetramethylpyrazine (TMP) is used for the treatment of ischemic stroke. However, the mechanism by which TMP regulates ferroptosis in CIRI is yet to be explored.

AEBP1 Silencing Protects Against Cerebral Ischemia/Reperfusion Injury by Regulating Neuron Ferroptosis and Microglia M2 Polarization Through PRKCA-PI3K-Akt Axis.

Cerebral ischemia/reperfusion injury is one of the main causes of neuronal damage. Neuron ferroptosis and microglia polarization are considered as critical processes during cerebral ischemia/reperfusion. Adipocyte enhancer-binding protein 1 (AEBP1) usually acts as a transcriptional repressor which is involved in various diseases.

A multiple targeting rapamycin and SS31 conjugate enhances ischemic stroke therapy.

Background: The identification of drugs targeting multiple pathways is essential for comprehensive protection against cerebral ischemia-reperfusion injury.

Research Design And Methods: This study aimed to develop RS31, a multi-target cytoprotectant composed of SS31 (an oxidative stress mitigator) and rapamycin (Rapa), contributes anti-inflammatory and blood-brain barrier protection. RS31 was synthesized using click chemistry, and its ability to scavenge reactive oxygen species (ROS) and reduce inflammation was tested in HO-injured PC12 cells and LPS-stimulated BV2 cells.

Role of BDNF-TrkB signaling in the improvement of motor function and neuroplasticity after ischemic stroke in rats by transcranial direct current stimulation.

Background: Transcranial direct current stimulation (tDCS) has an impact on improving cognitive and motor dysfunction induced by ischemia-reperfusion injury. However, to use this technology more rationally in clinical practice, a deepened understanding of the molecular mechanisms behind its therapeutic effects is needed. This study explored the role of the brain-derived neurotrophic factor(BDNF) and its associated receptor tropomyosin-receptor kinase B(TrkB) while deciphering the underlying mechanisms in transcranial direct current therapy to treat ischemic stroke.