Activation of GPER1 alleviates white matter injury by promoting microglia M2 polarization through EGFR/Stat3 pathway in intracerebral hemorrhage mice DOI Creative Commons
Xuyang Zhang, Jianchao Mao, Huanhuan Li

et al.

Journal of Stroke and Cerebrovascular Diseases, Journal Year: 2025, Volume and Issue: 34(6), P. 108315 - 108315

Published: April 12, 2025

White matter injury (WMI) is a major pathophysiological process after intracerebral hemorrhage (ICH). G protein-coupled estrogen receptor 1 (GPER1) has been validated to exert crucial role in regulating neuroinflammation and microglia polarization. Our previous report reveals activation of GPER1 improves the neurological deficits ICH via inhibition A1 astrocytes. However, on protection WMI modulation polarization remains unclear. In present study, mice model was induced by autologous whole blood injection vitro established treatment BV2 cells with FeSO4. Mice were treated agonist G1, antagonist G15 or EGFR inhibitor AG1478. Besides, conditional medium used intervene MO3.13 oligodendrocytes. Immunostaining, immunoblots, transmission electron microscope PI staining determine WMI, potential molecular mechanism ICH, respectively. data showed G1 ameliorated day 3 ICH. reduced release IL-1β, TNF-α increased produce IL-4, IL-10 as well shifting from proinflammatory M1 anti-inflammatory M2 phenotype vivo vitro. Meanwhile, alleviated oligodendrocytes death mitigating modulating Mechanistic study demonstrated EGFR/Stat3 signaling pathway involved Collectively, our findings through pathway.

Language: Английский

Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches DOI Creative Commons

Dmitriy Lapin,

Archna Sharma, Ping Wang

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Jan. 21, 2025

Abstract Central nervous system (CNS) injuries, such as ischemic stroke (IS), intracerebral hemorrhage (ICH) and traumatic brain injury (TBI), are a significant global burden. The complex pathophysiology of CNS is comprised primary secondary injury. Inflammatory incited by damage-associated molecular patterns (DAMPs) which signal variety resident cells infiltrating immune cells. Extracellular cold-inducible RNA-binding protein (eCIRP) DAMP acts through multiple non-immune to promote inflammation. Despite the well-established role eCIRP in systemic sterile inflammation, its less elucidated. Recent literature suggests that pleiotropic inflammatory mediator also being evaluated clinical biomarker indicate prognosis injuries. This review provides broad overview injury, with focus on immune-mediated neuroinflammation. We then what known about mechanisms both non-CNS cells, identifying opportunities for further study. explore eCIRP’s potential prognostic marker severity outcome. Next, we provide an eCIRP-targeting therapeutics suggest strategies develop these agents ameliorate Finally, emphasize exploring novel mechanisms, aside from neuroinflammation, critical therapeutic target

Language: Английский

Citations

2
Therapeutic Role of Microglia/Macrophage Polarization in Intracerebral Hemorrhage DOI Creative Commons
Raşit Dinç, Nurittin Ardıç

Clinical and Translational Neuroscience, Journal Year: 2025, Volume and Issue: 9(1), P. 4 - 4

Published: Jan. 20, 2025

Intracerebral hemorrhage (ICH) is a significant health problem with high mortality and morbidity rates, partly due to limited treatment options. Hematoma after ICH causes neurological deficits the mass effect. Hemorrhage catalyzes secondary damage, resulting in increased poor prognosis, problems. This review evaluates role of immunotherapeutic approaches based on original full-text articles pathophysiology immunotherapy ICH, emphasis modulation microglia/macrophage polarization M2 subtype. In this review, we concluded that injury progression complex multifaceted. Inflammation plays dominant injuries. Furthermore, cells involved inflammatory process have dual roles pro-inflammatory/destructive anti-inflammatory/healing. While inflammation makes immune system therapeutic target them can modulate Resident microglia (and even macrophages migrating from peripheral source) are important targets for because their initiation phase shaping immunity. Although clinical results remain poor, experimental trial data seem promising deciphering providing

Language: Английский

Citations

0
Identification of AIF1 as a protein target of notoginsenosides in brain tissue of mice with intracerebral hemorrhage based on hapten immunoaffinity fishing technique DOI Creative Commons
Feiyan Chen, Wei Qin,

Qianlin Li

et al.

Journal of Ginseng Research, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0
A prospective cohort study on serum PINK1 as a biochemical marker in relation to poor neurological prognosis, stroke-associated pneumonia and early neurological deterioration after acute intracerebral hemorrhage DOI
Wen‐Fei Ni,

Chen Si-hua,

Le Cao Dai

et al.

Clinica Chimica Acta, Journal Year: 2025, Volume and Issue: unknown, P. 120282 - 120282

Published: April 1, 2025

Language: Английский

Citations

0
Activation of GPER1 alleviates white matter injury by promoting microglia M2 polarization through EGFR/Stat3 pathway in intracerebral hemorrhage mice DOI Creative Commons
Xuyang Zhang, Jianchao Mao, Huanhuan Li

et al.

Journal of Stroke and Cerebrovascular Diseases, Journal Year: 2025, Volume and Issue: 34(6), P. 108315 - 108315

Published: April 12, 2025

White matter injury (WMI) is a major pathophysiological process after intracerebral hemorrhage (ICH). G protein-coupled estrogen receptor 1 (GPER1) has been validated to exert crucial role in regulating neuroinflammation and microglia polarization. Our previous report reveals activation of GPER1 improves the neurological deficits ICH via inhibition A1 astrocytes. However, on protection WMI modulation polarization remains unclear. In present study, mice model was induced by autologous whole blood injection vitro established treatment BV2 cells with FeSO4. Mice were treated agonist G1, antagonist G15 or EGFR inhibitor AG1478. Besides, conditional medium used intervene MO3.13 oligodendrocytes. Immunostaining, immunoblots, transmission electron microscope PI staining determine WMI, potential molecular mechanism ICH, respectively. data showed G1 ameliorated day 3 ICH. reduced release IL-1β, TNF-α increased produce IL-4, IL-10 as well shifting from proinflammatory M1 anti-inflammatory M2 phenotype vivo vitro. Meanwhile, alleviated oligodendrocytes death mitigating modulating Mechanistic study demonstrated EGFR/Stat3 signaling pathway involved Collectively, our findings through pathway.

Language: Английский

Citations

0