Baicalin Reduces Immune Cell Infiltration by Inhibiting Inflammation and Protecting Tight Junctions in Ischemic Stroke Injury

The American Journal of Chinese Medicine, Год журнала: 2023, Номер 51(02), С. 355 - 372

Опубликована: Янв. 1, 2023

Ischemic stroke is a serious health hazard that lacks effective treatment strategies. This study aims to investigate baicalin’s effect on tight junctions and immune cell infiltration after ischemic injury. Rat brain microvascular endothelial cells (BMECs) were treated with OGD/R establish an in vitro model. Caspase-3, Bax, Bcl-2, zonula occludens-1 (ZO-1), occludin, claudin-5, tumor necrosis factor (TNF)-[Formula: see text], interleukin (IL)-6, inducible nitric oxide synthase (iNOS), Toll-like receptor (TLR) 2, TLR4, nuclear factor-kappa B (NF-[Formula: text]B) expressions detected using qRT-PCR western blotting. ZO-1, TNF-[Formula: iNOS, IL6, CD31, ZO-1 examined immunofluorescence. A tube formation assay was performed measure angiogenesis. An ischemia-reperfusion model rats established by middle cerebral artery occlusion. The infarct volume observed 2,3,5-triphenyltetrazolium chloride staining. IL6 levels the serum tested ELISA. Flow cytometry examine inflammatory infiltration. Baicalin had no significant proliferation of normal BMECs. inhibited apoptosis, protected against junction injury, alleviated response OGD/R-induced BMECs IR rats, highest dose (25[Formula: text][Formula: text]g/mL) exerting superior effect. decreased neurological function score, volume, water content, relieved morphological changes, vivo. In conclusion, baicalin could reduce protect junctions, resist infiltration, thereby alleviating stroke. Our findings potentially provide novel strategy for

Язык: Английский

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The Role of miRNAs in Dexmedetomidine’s Neuroprotective Effects against Brain Disorders

International Journal of Molecular Sciences, Год журнала: 2022, Номер 23(10), С. 5452 - 5452

Опубликована: Май 13, 2022

There are limited neuroprotective strategies for various central nervous system conditions in which fast and sustained management is essential. Neuroprotection-based therapeutics have become an intensively researched topic the neuroscience field, with multiple novel promising agents, from natural products to mesenchymal stem cells, homing peptides, nanoparticles-mediated all aiming significantly provide neuroprotection experimental clinical studies. Dexmedetomidine (DEX), α2 agonist commonly used as anesthetic adjuvant sedation opioid-sparing medication, stands out this context due its well-established effects. Emerging evidence preclinical studies suggested that DEX could be protect against cerebral ischemia, traumatic brain injury (TBI), spinal cord injury, neurodegenerative diseases, postoperative cognitive disorders. MicroRNAs (miRNAs) regulate gene expression at a post-transcriptional level, inhibiting translation of mRNA into functional proteins. In vivo vitro deciphered brain-related miRNAs dysregulated miRNA profiles after several disorders, including TBI, ischemic stroke, Alzheimer's disease, sclerosis, providing emerging new perspectives therapy by modulating these miRNAs. Experimental revealed some effects mediated miRNAs, counteracting mechanisms disease models, such lipopolysaccharides induced neuroinflammation, β-amyloid dysfunction, ischemic-reperfusion anesthesia-induced neurotoxicity models. This review aims outline disorders We address targeting ameliorating anesthetics, reducing improving diseases.

Язык: Английский

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Astrocyte‐like subpopulation of NG2 glia in the adult mouse cortex exhibits characteristics of neural progenitor cells

Glia, Год журнала: 2023, Номер 72(2), С. 245 - 273

Опубликована: Сен. 29, 2023

Abstract Glial cells expressing neuron‐glial antigen 2 (NG2), also known as oligodendrocyte progenitor (OPCs), play a critical role in maintaining brain health. However, their ability to differentiate after ischemic injury is poorly understood. The aim of this study was investigate the properties and functions NG2 glia brain. Using transgenic mice, we selectively labeled NG2‐expressing progeny both healthy focal cerebral ischemia (FCI). single‐cell RNA sequencing, classified glial into five distinct subpopulations based on gene expression patterns. Additionally, examined membrane these using patch‐clamp technique. Of identified subpopulations, three were OPCs, whereas fourth subpopulation had characteristics indicative likely develop oligodendrocytes. fifth showed astrocytic markers similarities neural cells. Interestingly, present post‐ischemic tissue; however, its profile changed ischemia, with increased numbers genes related neurogenesis. Immunohistochemical analysis confirmed temporal neurogenic an presence positive for Purkinje cell protein‐4 at periphery lesion 12 days FCI, well NeuN‐positive 28 60 injury. These results suggest potential development neuron‐like arising from tissue. Our provides insights plasticity capacity neurogenesis stroke.

Язык: Английский

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Plasma microRNA Levels After Electroconvulsive Therapy in Treatment-Resistant Depressed Patients

Journal of Ect, Год журнала: 2025, Номер unknown

Опубликована: Янв. 7, 2025

Objectives Electroconvulsive therapy (ECT) is one of the most effective treatments for treatment-resistant depression (TRD), even though molecular mechanisms underlying its efficacy remain largely unclear. This study aimed, first time, to analyze plasma levels miRNAs, key regulators gene expression, in TRD patients undergoing ECT investigate potential changes during treatment and their associations with symptom improvement. Methods The involved 27 who underwent ECT. Plasma samples were collected at baseline (T0) 1 month after last session (T1), miRNA analysis was conducted by qRT-PCR. We also performed prediction miRNAs differentially expressed KEGG pathway analysis. Results miR-95-3p, miR-194-5p, miR-324-3p, miR-195-5p, miR-19b-3p, miR-30c-5p, let-7i-5p, miR-497-5p nominally downregulated T1. Changes miR-324-3p miR-30c-5p between T0 T1 significantly correlated Among predicted target genes these 2 we noticed presence VEGF SIRT1, whose expression regulation has been associated mechanism action previous studies. Conclusions study's relevant results are related correlation reductions improvement symptoms response ECT, positioning as promising candidates further These findings support extend clinical preclinical research indicating a role action. However, no significant effects modulation observed, highlighting need future replications broader confirm results.

Язык: Английский

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Brain-targeted delivery of Acetyl-11-Keto-β-Boswellic acid with enhanced anti-inflammatory efficacy via blood-brain barrier peptide shuttle PepH3

Chemical Engineering Journal, Год журнала: 2025, Номер 509, С. 160664 - 160664

Опубликована: Фев. 19, 2025

Язык: Английский

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Dexmedetomidine activates mitophagy and protects against pyroptosis in oxygen-glucose deprivation/reperfusion-induced brain damage via PINK1/Parkin pathway activation

Journal of Bioenergetics and Biomembranes, Год журнала: 2025, Номер unknown

Опубликована: Фев. 22, 2025

Язык: Английский

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Neuroprotective effects of GPR68 against cerebral ischemia-reperfusion injury via the NF-κB/Hif-1α pathway

Brain Research Bulletin, Год журнала: 2024, Номер 216, С. 111050 - 111050

Опубликована: Авг. 13, 2024

G protein-coupled receptor 68 (GPR68), an orphan receptor, has emerged as a promising therapeutic target for mitigating neuronal inflammation and oxidative damage. This study explores the protective mechanisms of GPR68 in cerebral ischemia-reperfusion injury (CIRI).

Язык: Английский

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Knockdown of circular RNA tousled-like kinase 1 relieves ischemic stroke in middle cerebral artery occlusion mice and oxygen-glucose deprivation and reoxygenation-induced N2a cell damage

Bioengineered, Год журнала: 2022, Номер 13(2), С. 3434 - 3449

Опубликована: Янв. 22, 2022

Ischemic stroke (IS) is an essential contributor to the neurological morbidity and mortality throughout world. The significance of circular RNA tousled-like kinase 1 (circTLK1) in IS has been documented. This study set out explore mechanism circTLK1 IS. Middle cerebral artery occlusion (MCAO) mouse models vivo oxygen-glucose deprivation reoxygenation (OGD/R) cell vitro were first established, followed by evaluation infarct volume impairment, viability apoptosis. expression patterns circTLK1, miR-26a-5p, phosphatase tensin homolog (PTEN), insulin-like growth factor type receptor (IGF-1 R), glucose transporter (GLUT1) detected RT-qPCR Western blotting. Co-localization miR-26a-5p N2a cells was tested fluorescence situ hybridization assay. binding relationships among PTEN, verified dual-luciferase assay pull-down. PTEN highly expressed while under-expressed models. knockdown decreased impairment MCAO relieved OGD/R-induced neuronal injury vitro. co-located cytoplasm. regulated as a sponge miR-26a-5p. positively IGF-1 R GLUT1 expressions. inhibitor annulled repressive effects silencing on injury. sh-PTEN partially In conclusion, via miR-26a-5p/PTEN/IGF-1 R/GLUT1 axis. These results may provide new direction potential therapeutic targets.

Язык: Английский

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Effects of Dexmedetomidine on Perioperative Brain Protection in Elderly Frail Patients

Journal of Anesthesia and Translational Medicine, Год журнала: 2023, Номер 2(3), С. 29 - 33

Опубликована: Янв. 1, 2023

With the rapid growth of elderly population and advancements in surgical anesthesia techniques, an increasing number patients are opting for surgery.Among them, frail is on rise.Perioperative neurocognitive disorders common complications patients, which significantly impact their rehabilitation quality life.Dexmedetomidine a highly effective selective α2-adrenergic receptor agonist with sedative, analgesic, anti-sympathetic, non-respiratory depressant properties.It can reduce incidence postoperative delirium cognitive dysfunction.However, its perioperative brain protection effect frailty remains unclear, further extensive studies required to explore this future.

Язык: Английский

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Mechanism of lncRNA SNHG16 in oxidative stress and inflammation in oxygen-glucose deprivation and reoxygenation-induced SK-N-SH cells

Bioengineered, Год журнала: 2022, Номер 13(3), С. 5021 - 5034

Опубликована: Фев. 16, 2022

Cerebral ischemia-reperfusion injury imposes a clinical challenge for physicians in the wake of ischemic stroke. Meanwhile, recent evidence has come to light eliciting neuroprotective function SNHG16 cerebrovascular diseases. Accordingly, current study sought analyze regulatory mechanism long non-coding RNA small nucleolar host gene16 (SNHG16) oxidative stress (OS) and cell inflammation. Firstly, models oxygen-glucose deprivation reoxygenation (OGD/R) were established SK-N-SH cells. Cell proliferation apoptosis appraised using counting kit-8 flow cytometry. Additionally, SNHG16, X-linked inhibitor protein (XIAP), microRNA (miR-421), reactive oxygen species (ROS), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor -α, interleukin (IL)-1β, IL-10 expression patterns determined. In addition, we determined validated subcellular localization binding relationships between miR-421, miR-421 XIAP. It was found that poorly-expressed OGD/R-treated On other hand, over-expression enhanced proliferation, inhibited apoptosis, alleviated OS Furthermore, bound facilitate Up-regulation or down-regulation XIAP could reverse suppressive effects on Collectively, our findings indicated expression, thus alleviating inflammation OGD/R-induced

Язык: Английский

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