α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen-Glucose Deprivation/Reoxygenation.

Elevated inflammatory reactions are a significant component in cerebral ischemia-reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen-glucose deprivation/reoxygenation (OGDR) condition.

SENP6-Mediated deSUMOylation of Nrf2 Exacerbates Neuronal Oxidative Stress Following Cerebral Ischemia and Reperfusion Injury.

Oxidative stress is believed to play critical pathophysiological roles in ischemic brain injury, and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is recognized as the most crucial endogenous antioxidant stress damage route. Some research have demonstrated that Nrf2 play critical roles in oxidative stress after ischemic stroke, but the underlying mechanism are not fully elucidated. This study reveals that Nrf2 is modified by SUMOylation and identifies Sentrin/SUMO-specific protease 6 (SENP6) as a negative regulator of Nrf2 SUMOylation.

Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis.

Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury.

Hydrogen sulfide-mediated inhibition of ROCK exerts a vasoprotective effecton ischemic brain injury.

As a gas molecule, hydrogen sulfide (HS) exerts neuroprotective effects. Despite its recognized importance, there remains a need for a deeper understanding of HS's impact on vascular smooth muscle cells and its role in ischemic brain injury. This study employs encompassing cultured primary cerebral vascular smooth muscle cells, oxygen-glucose deprivation/reoxygenation model, in vitro vascular tone assessments, in vivo middle cerebral artery occlusion and reperfusion experimentation in male rats, and the utilization of ROCK knockout, to unravel the intricate relationship between H2S and cerebrovascular diastolic function.

Ku70 silencing aggravates oxygen-glucose deprivation/reperfusion-induced injury by activation of the p53 apoptotic pathway in rat cortical astrocytes.

Oxidative stress-induced DNA damage is an important mechanism that leads to the death of neuronal cells after ischemic stroke. Our previous study found that Ku70 was highly expressed in ischemic brain tissue of rats after cerebral ischemia-reperfusion injury. However, the role of Ku70 in glucose-oxygen deprivation/reperfusion (OGD/R) in astrocytes has not been reported.

Utilizing network pharmacology, pharmacodynamics, molecular biology studies, and molecular docking techniques to uncover the mechanism of the Ligusticum wallichii-borneol medication combination for the treatment of ischemic stroke in rat models.

Objective: To use pharmacodynamics, molecular biology studies, network pharmacology, and molecular docking to study the mechanism of action of the Ligusticum wallichii (known as Chuanxiong in China, CX) and borneol (known as Bingpian in China, BP) medication pair (CXBP) for the treatment of ischemic stroke.

Methods: The TCMSP, ETCM, and SymMap databases provided the effective chemical components and targets of CXBP, while the databases OMIM, GeneCards, TTD, Pubmed, Web of Science, CNKI, Wanfang Data, and VIP Database provided targets relevant to ischemic stroke. In addition we conducted animal experiments for validation.

Ferroptosis and its impact on common diseases.

Ferroptosis is a novel form of programmed cell death characterized by iron accumulation, lipid peroxidation, and a decline in antioxidant capacity, all of which are regulated by gene expression. The onset of numerous diseases is closely associated with ferroptosis. Common diseases affect a large population, reduce the quality of life, and impose an increased burden on the healthcare system.

Adequate post-ischemic reperfusion of the mouse brain requires endothelial NFAT5.

Severity and outcome of strokes following cerebral hypoperfusion are significantly influenced by stress responses of the blood vessels. In this context, brain endothelial cells (BEC) regulate inflammation, angiogenesis and the vascular resistance to rapidly restore perfusion. Despite the relevance of these responses for infarct volume and tissue recovery, their transcriptional control in BEC is not well characterized.

KLF6 silencing attenuates MCAO-induced brain injury and cognitive dysfunction via targeting ferroptosis and activating the Nrf2/HO-1 pathway.

Introduction: The incidence of cerebral ischemia-reperfusion injury (I/R) is complex which seriously threatens the life safety of patients. Neither its prevention nor its treatment has been successful so far. Proteins that bind to DNA and belong to the C2/H2 zinc finger family are known as Krüppel-like factors (KLFs).

Sodium ferulate attenuates ischaemic stroke by mediating the upregulation of thrombospondin-4 expression and combined treatment with bone marrow mesenchymal stem cells.

Ischaemic stroke is one of the major diseases affecting human health, involving complex and diverse pathological mechanisms, including inflammatory response, oxidative stress and angiogenesis. Sodium ferulate (SF) exerts a protective effect on cerebral ischaemia/reperfusion and when combined with bone marrow mesenchymal stem cells (BMSCs), has a considerable therapeutic effect on brain injury in rats. Here, we speculate that SF also exerts cerebroprotective effects.

Oxygen-glucose-deprived peripheral blood mononuclear cells act on hypoxic lesions after ischemia-reperfusion injury.

Background: Despite advances in reperfusion therapies, ischemic stroke remains a major cause of long-term disability due to residual hypoxic lesions persisting after macrovascular reperfusion. These residual hypoxic lesions, caused by microvascular dysfunction, represent an important therapeutic target. We previously demonstrated that oxygen-glucose-deprived peripheral blood mononuclear cells (OGD-PBMCs) migrate to ischemic brain regions and promote functional recovery after stroke.

Buyang Huanwu Decoction prevents hemorrhagic transformation after delayed t-PA infusion via inhibiting NLRP3 inflammasome/pyroptosis associated with microglial PGC-1α.

Ethnopharmacological Relevance: Delayed tissue-type plasminogen activator (t-PA) thrombolysis, which has a restrictive therapeutic time window within 4.5 h following ischemic stroke (IS), increases the risk of hemorrhagic transformation (HT) and subsequent neurotoxicity. Studies have shown that the NLRP3 inflammasome activation reversely regulated by the PGC-1α leads to microglial polarization and pyroptosis to cause damage to nerve cells and the blood-brain barrier.

Halcinonide activates smoothened to ameliorate ischemic stroke injury.

Objectives: The Shh pathway may shed new light on developing new cell death inhibitors for the therapy of ischemic stroke. We aimed to examine whether the Shh co-reporter SMO or its agonist halcinonide can upregulate Bcl-2 to suppress neuronal cell death, ultimately improving behavioral deficits and reducing cerebral infarction in an ischemic stroke model.

Methods: Halcinonide or genetic manipulation of SMO was conducted in PC12 cells to examine their impacts on oxidative or OGD/R stress, and the chemical, along with AAV-SMO or AAV-EGFP were tested in MCAO rats to investigate their potential protective effects against neuronal damages due to cerebral I/R injury.

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.

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.