Quercetin is a potential therapy for post-infarction NETosis formation.

The surgical intervention during myocardial infarction (MI) is associated with the risk of reperfusion injury, infiltration of tissues with polymorphonuclear neutrophils, and neutrophil extracellular trap (NET) formation. We hypothesized that inhibition of NETs with the use of quercetin might be a promising cardioprotective strategy. Wistar rats underwent LAD occlusion (MI) for 40 min followed by 90 min of reperfusion.

Bilateral transcranial direct-current stimulation confers neuroprotection through suppression of PKM2 after mouse cerebral ischemia injury.

Background: In its tetrameric form, pyruvate kinase M2 isoform (PKM2) catalyzes the last step of glycolysis and plays a key role in the metabolic reprogramming via regulating the signaling of pentose phosphate pathway (PPP). But the role of PKM2 in cerebral ischemia-reperfusion (I/R) injury remains unknown.

Methods: Mice model of middle cerebral artery occlusion (MCAO) and model of oxygen-glucose deprivation (OGD) injury in cultured neurons were established.

Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.

Ischemic stroke is a leading cause of disability and mortality worldwide, with current therapies limited in addressing its complex pathophysiological mechanisms, such as inflammation, oxidative stress, apoptosis, and impaired autophagy. Glycyrrhizic acid (GA), a bioactive compound from licorice ( L.), has demonstrated neuroprotective properties in preclinical studies.

LncRNA Taurine Up-Regulated 1 Knockout Provides Neuroprotection in Ischemic Stroke Rats by Inhibiting Nuclear-Cytoplasmic Shuttling of HuR.

: Long non-coding RNA taurine-upregulated gene 1 (TUG1) is involved in various cellular processes, but its role in cerebral ischemia-reperfusion injury remains unclear. This study investigated TUG1's role in regulating the nucleocytoplasmic shuttling of human antigen R (HuR), a key apoptosis regulator under ischemic conditions. : CRISPR-Cas9 technology was used to generate TUG1 knockout Sprague Dawley rats to assess TUG1's impact on ischemic injury.

Efficacy of Omega-5 NanoPSO Treatment in the Hippocampus, Through Antioxidant Mechanisms, After an Ischemia/Reperfusion Injury, in Murine Model.

Stroke is the third cause of death worldwide and a health problem, and current therapy continues to be very poor. It promotes an alteration associated with excitotoxicity, oxidative stress, and inflammatory processes, exacerbating the damage in the brain. Although cortical areas are the most affected by stroke, the hippocampus can be impacted in the long term through the pathways it connects with these areas, which are associated further with motor alterations; this encourages the search for new therapeutic approaches.

Exacerbated ischemic brain damage in type 2 diabetes via methylglyoxal-mediated miR-148a-3p decline.

Background: Although microvascular dysfunction is a widespread phenomenon in type 2 diabetes (T2D) and is recognized as a main cause of T2D-aggravated ischemic stroke injury, the underlying mechanisms by which T2D-mediated exacerbation of cerebral damage after ischemic stroke is still largely uncharacterized. Here, we found that methylglyoxal-mediated miR-148a-3p decline can trigger blood-brain barrier dysfunction, thereby exacerbating cerebrovascular injury in diabetic stroke.

Methods: Using T2D models generated with streptozotocin plus a high-fat diet or db/db mice, and then inducing focal ischemic stroke through middle cerebral artery occlusion and reperfusion (MCAO/R), we established a diabetic stroke mouse model.

Transplantation of human neural stem cells repairs neural circuits and restores neurological function in the stroke-injured brain.

Exogenous neural stem cell (NSC) transplantation has become one of the most promising treatment methods for chronic stroke. Recent studies have shown that most ischemia-reperfusion model rats recover spontaneously after injury, which limits the ability to observe long-term behavioral recovery. Here, we used a severe stroke rat model with 150 minutes of ischemia, which produced severe behavioral deficiencies that persisted at 12 weeks, to study the therapeutic effect of neural stem cells on neural restoration in chronic stroke.

M1 Microglia-Derived Exosomes Promote A1 Astrocyte Activation and Aggravate Ischemic Injury via circSTRN3/miR-331-5p/MAVS/NF-κB Pathway.

Background: After ischemic stroke (IS), microglia and astrocytes undergo polarization, transforming into a pro-inflammatory phenotype (M1 or A1). According to previous studies, exosomes might play an important role in the interplay between M1 microglia and A1 astrocytes after IS.

Methods: We used the microglial oxygen-glucose deprivation/reperfusion (OGD/R) model and ultracentrifugation to extract M1 microglial exosomes (M1-exos).

Panax notoginseng saponins promotes angiogenesis after cerebral ischemia-reperfusion injury.

Background: Ischemic stroke is a devastating disease that can result in permanent disability and death, and angiogenesis plays a critical role in the recovery and survival of patients and animal models of ischemic stroke. Panax notoginseng has been used as a key herb in the treatment of stroke diseases due to its effect in promoting blood circulation and removing blood stasis. However, the role of Panax notoginseng saponins, in promoting angiogenesis is unclear.

Ethanol extracts of Cinnamomum migao H.W. Li attenuates neuroinflammation in cerebral ischemia-reperfusion injury via regulating TLR4-PI3K-Akt-NF-κB pathways.

Ethnopharmacological Relevance: Cinnamomum migao H.W. Li, commonly known as migao (MG), is used in the Miao region of China for treating cardiovascular and cerebrovascular diseases, attributed to its detoxifying (Jiedu in Chinese), activating blood circulation (Huoxue in Chinese), and promoting Qi circulation (Tongqi in Chinese) properties.

Design and Synthesis of Butylphthalide-Hydroxycinnamic Acid Hybrid Derivatives as Potential Antiplatelet Agents.

Thirty-eight novel butylphthalide-hydroxycinnamic acid hybrid derivatives were designed and synthesized to discover effective antiplatelet agglutination drugs. Among these compounds, 3 o gave the optimal inhibitory activity against AA-induced platelet aggregation in vitro and also exhibited better inhibition than the precursor 3-n-butylphthalide (NBP) against thrombin-induced platelet contraction, carrageenan-induced tail thrombosis, and FeCl-induced common carotid artery thrombosis. Further investigations on the anti-ischemic stroke activity revealed that compound 3 o exhibited a remarkable protective effect against ischemic/reperfusion brain injury.

Chaperone-Mediated Autophagy Alleviates Cerebral Ischemia-Reperfusion Injury by Inhibiting P53-Mediated Mitochondria-Associated Apoptosis.

Ischemia-reperfusion is a complex brain disease involving multiple biological processes, including autophagy, oxidative stress, and mitochondria-associated apoptosis. Chaperone-mediated autophagy (CMA), a selective autophagy, is involved in the development of various neurodegenerative diseases and acute nerve injury, but its role in ischemia-reperfusion is unclear. Here, we used middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R) models to simulate cerebral ischemic stroke in vivo and in vitro, respectively.

Ginsenoside Rb3 Promotes Opa1-Mediated Regenerative Neurogenesis via Activating the Ido1 Pathway in Ischemic Stroke.

The activation of neural stem cells (NSCs) residing in the subventricular zone (SVZ) and dentate gyrus (DG) has been shown to promote the restoration of damaged brain tissues. Ginsenoside Rb3 (Rb3) is a bioactive substance known for its pharmacological properties in treating neurological disorders. This study investigated the effects of Rb3 on neural regeneration following ischaemic stroke (IS) and the underlying mechanisms involved.

Exploration the effective components of Gastrodia elata in improving cerebral ischemia reperfusion injury based on "Spectrum-effect" correlation and zebrafish verification experiment.

Background: Gastrodia elata (GE) has been widely used in clinical practice for many years with the functions of relieving stroke, suppressing liver Yang, dispelling wind and clearing collaterals. Our group's previous experimental studies have proved that GE has therapeutic effect on cerebral ischemia reperfusion injury (CIRI) (Ding et al., 2022).

Astragalus polysaccharide treatment relieves cerebral ischemia‒reperfusion injury by promoting M2 polarization of microglia by enhancing O-GlcNAcylation.

Cerebral ischemia‒reperfusion (I/R) injury seriously threatens the lives of patients. Astragalus polysaccharide (APS) is the main active ingredient of Astragalus membranaceus and has a wide range of pharmacological activities. Here, we aimed to explore the impacts of APS on cerebral I/R injury and its specific mechanisms.

KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11.

Ischemic stroke poses a significant global health risk. Currently, recanalization of blood flow through surgery or medication is the only effective means to control ischemia-reperfusion injury. This study aims to explore the role and molecular mechanism of OGT in regulating neuronal injury and motor deficits following a stroke.

20(R)-ginsenoside Rg3 protects against focal cerebral ischemia‒reperfusion injury by suppressing autophagy via PI3K/Akt/mTOR signaling pathway.

Objective: This study aimed to investigate the effect of 20(R)-ginsenoside Rg3 on autophagy induced by cerebral ischemia‒reperfusion injury (CIRI) in rats and explore its regulation of the PI3K/Akt signaling pathway.

Methods: Middle cerebral artery occlusion/reperfusion (MCAO/R) in male rats was injected intraperitoneally with 20(R)-ginsenoside Rg3 (5, 10, 20 mg/kg) 12 h before modeling, 2 h after ischemia and 12 h after reperfusion. Neurobehavioral and neuronal morphological changes were detected 24 h after brain I/R.

Epicatechin-mediated modulation of the Nrf2/HO-1 pathway alleviates senile cerebral ischemic/reperfusion injury.

Excessive reactive oxygen species (ROS) generated during cerebral ischemic reperfusion (CIRI) are crucial for subsequent tissue damage. However, despite the potential benefits of antioxidants reported in clinical applications, few have proven effective in treating CIRI, particularly in the elderly. Epicatechin (EC) is a catechol flavonoid monomer derived from natural tea plants.

Targeting CD36 With EP 80317 Reduces Remote Inflammatory Response to Hind Limb Ischemia-Reperfusion in Mice.

Reperfusion of ischemic skeletal muscle triggers oxidative stress and an immediate inflammatory reaction, leading to damage of distant organs such as the lungs. The inflammatory process implicates numerous mediators, including cytokines, chemokines, and arachidonic acid metabolites. In the orchestration of the inflammatory cascade, a critical role is played by the cluster of differentiation-36 receptor (CD36), a scavenger receptor class B protein (SR-B2) which is expressed on macrophages and functions as a Toll-like receptor coreceptor.