Astragaloside IV promotes cerebral tissue restoration through activating AMPK- mediated microglia polarization in ischemic stroke rats

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 334, P. 118532 - 118532

Published: July 6, 2024

Language: Английский

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Exploring the active components and potential mechanisms of Zhimu-Huangbai herb-pair in the treatment of depression

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156365 - 156365

Published: Jan. 1, 2025

Language: Английский

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Galectin‐1 Regulates Inflammatory Responses and Promotes Microglial M2 Polarization in Chronic Migraine

European Journal of Neuroscience, Journal Year: 2025, Volume and Issue: 61(3)

Published: Feb. 1, 2025

Chronic migraine (CM) is a severe and debilitating neurological disorder with an unclear pathophysiology. Galectin-1, β-galactoside-binding protein, known for its anti-inflammatory immune-regulatory effects in various inflammation-related diseases. However, role CM has not been fully elucidated. In this study, we analysed data from patients employed nitroglycerin-induced mouse model to explore the potential of galectin-1. Serum galectin-1 levels were significantly lower compared healthy controls. Additionally, negatively correlated Visual Analogue Scale (VAS) Headache Impact Test (HIT-6) scores. also exhibited elevated IL-6 TNF-α reduced IL-10. Notably, inversely positively model, expression was spinal trigeminal nucleus caudalis (Sp5C) region. Supplementation increased paw periorbital mechanical thresholds light aversion anxiety-like behaviours. Moreover, enhanced microglial morphology, promoted M2 polarization, pro-inflammatory factors cytokine Mechanistically, on microglia may involve activation PI3K/AKT signalling pathway, as evidenced by phosphorylation PI3K AKT. summary, our study demonstrates that plays crucial pathogenesis chronic migraine. Exogenous supplementation effectively alleviates symptoms promotes suggesting represent novel therapeutic target CM.

Language: Английский

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GDF11 Mitigates Neuropathic Pain via Regulation of Microglial Polarization and Neuroinflammation through TGF-βR1/SMAD2/NF-κB Pathway in Male Mice

Journal of Neuroimmune Pharmacology, Journal Year: 2025, Volume and Issue: 20(1)

Published: Feb. 12, 2025

Language: Английский

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Circular RNA APP contributes to Alzheimer’s disease pathogenesis by modulating microglial polarization via miR-1906/CLIC1 axis

Alzheimer s Research & Therapy, Journal Year: 2025, Volume and Issue: 17(1)

Published: Feb. 14, 2025

Abstract Background Abnormal microglial polarization phenotypes contribute to the pathogenesis of Alzheimer’s disease (AD). Circular RNAs (circRNAs) have garnered increasing attention due their significant roles in human diseases. Although research has demonstrated differential expression circRNAs AD, specific functions AD remain largely unexplored. Methods CircRNA microarray was performed identify differentially expressed hippocampus APP/PS1 and WT mice. The stability circAPP assessed via RNase R treatment assay. CircAPP downstream targets miR-1906 chloride intracellular channel 1 (CLIC1) were identified using bioinformatics proteomics, respectively. RT-PCR assay conducted detect circAPP, CLIC1. Morris water maze (MWM) test, passive avoidance test novel object recognition task used cognitive function Microglial M1/M2 pathology Western blot, flow cytometry Golgi staining assays. CLIC1 activity evaluated blot functional assays, subcellular location FISH RNA pull-down interaction with 3’ untranslated region (3’UTR) mRNA. Results In this study, we a circRNA, named that is encoded by amyloid precursor protein (APP) implicated AD. stable circRNA upregulated Aβ-treated cells Downregulation or CLIC1, overexpression microglia modulated mice, improved Further results revealed mainly distributed cytoplasm, could regulate interacting affecting expression, thereby regulating Conclusions Taken together, our study elucidates regulatory role miR-1906/CLIC1 axis, suggests may act as critical player represent promising therapeutic target for

Language: Английский

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Novel Insights into Neuroinflammatory Mechanisms in Traumatic Brain Injury: Focus on Pattern Recognition Receptors as Therapeutic Targets

Cytokine & Growth Factor Reviews, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

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β-elemene promotes microglial M2-like polarization against ischemic stroke via AKT/mTOR signaling axis-mediated autophagy

Chinese Medicine, Journal Year: 2024, Volume and Issue: 19(1)

Published: June 15, 2024

Abstract Background Resident microglia- and peripheric macrophage-mediated neuroinflammation plays a predominant role in the occurrence development of ischemic stroke. Microglia undergo polarization to M1/M2-like phenotype under stress stimulation, which mediates intracellular inflammatory response. β-elemene is natural sesquiterpene possesses potent anti-inflammatory activity. This study aimed investigate efficacy mechanism stroke from perspective balancing microglia polarization. Methods The middle cerebral artery occlusion (MCAO) model photothrombotic were established explore regulation effect on injury. LPS IFN-γ stimulated BV-2 cells used demonstrate effects potential regulating vitro. Results In C57BL/6 J mice subjected MCAO model, attenuated neurological deficit, reduced infarction volume neuroinflammation, thus improving promoted transformation M1-like M2-like, prevented neurons oxygen glucose deprivation/reoxygenation (OGD/R) injury by inhibiting factor release, thereby reducing neuronal apoptosis. Mechanically, activation TLR4/NF-κΒ MAPK signaling pathway increased AKT/mTOR mediated-autophagy, promoting M2-like microglia. Conclusions These results indicated that improved at least part, through AKT/mTOR-mediated autophagy. demonstrated might serve as promising drug for alleviating

Language: Английский

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CD300LF⁺ microglia impede the neuroinflammation following traumatic brain injury by inhibiting STING pathway

CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(7)

Published: July 1, 2024

The diversity in microglial phenotypes and functions following traumatic brain injury (TBI) is poorly characterized. aim of this study was to explore precise targets for improving the prognosis TBI patients from a perspective.

Language: Английский

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Chitosan-Rapamycin Carbon Dots Alleviate Glaucomatous Retinal Injury by Inducing Autophagy to Promote M2 Microglial Polarization

International Journal of Nanomedicine, Journal Year: 2024, Volume and Issue: Volume 19, P. 2265 - 2284

Published: March 1, 2024

Introduction: Glaucoma is a prevalent cause of irreversible vision impairment, characterized by progressive retinal ganglion cells (RGCs) loss, with no currently available effective treatment.Rapamycin (RAPA), an autophagy inducer, has been reported to treat glaucoma in rodent models promoting RGC survival, but its limited water solubility, systemic toxicity, and pre-treatment requirements hinder potential clinical applications.Methods: Chitosan (CS)-RAPA carbon dot (CRCD) was synthesized via hydrothermal carbonization CS RAPA transmission electron microscopy, Fourier transform infrared spectra, proton nuclear magnetic resonance.In vitro assays on human umbilical cord vein endothelial rat cell line examined biocompatibility anti-oxidative capabilities, while lipopolysaccharide-stimulated murine microglia (BV2) measured effects microglial polarization.In vivo, using mouse ischemia/reperfusion (I/R) model acute intraocular pressure elevation, the CRCD visual function, apoptosis, oxidative stress, M2 polarization were examined.Results: exhibited good solubility form free radical scavenging.In vitro, bio-compatible lowered which also found vivo I/R model.Additionally, both BV2 model, able promote activating autophagy, which, turn, down-regulated pro-inflammatory cytokines, such as IL-1β TNF-α, well up-regulated anti-inflammatory IL-4 TGF-β.All these ultimately aided preserving RGCs, subsequently, improved function.Discussion: could serve novel treatment strategy for glaucoma, incorporating into CDs, turn not only mitigating toxic side enhancing therapeutic efficacy.

Language: Английский

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New Insight into Neuropathic Pain: The Relationship between α7nAChR, Ferroptosis, and Neuroinflammation

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6716 - 6716

Published: June 18, 2024

Neuropathic pain, which refers to pain caused by a lesion or disease of the somatosensory system, represents wide variety peripheral central disorders. Treating neuropathic is quite demanding, primarily because its intricate underlying etiological mechanisms. The nervous system relies on microglia maintain balance, as they are associated with serving primary immune responses in brain next cell communication. Ferroptosis, driven phospholipid peroxidation and regulated iron, vital mechanism death regulation. Neuroinflammation can be triggered ferroptosis microglia, contributes release inflammatory cytokines. Conversely, neuroinflammation induce iron accumulation resulting microglial ferroptosis. Accumulating evidence suggests that neuroinflammation, characterized glial activation substances, significantly exacerbates development pain. By inhibiting ferroptosis, it may possible prevent subsequently alleviate homopentameric α7 subtype neuronal nicotinic acetylcholine receptor (α7nAChR) has potential suppress activation, transitioning M1 an M2 phenotype, facilitating anti-inflammatory factors, ultimately reducing Recent years have witnessed growing recognition regulatory role α7nAChR could target for treating This review summarizes mechanisms related progress according recent research. Such exploration will help elucidate relationship between α7nAChR, provide new insights into management.

Language: Английский

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