Neuroprotective effect of lipoxin A(4) methyl ester (LXA(4) ME) was tested in a rat model of permanent middle cerebral artery occlusion. LXA(4) ME was administrated through intracerebroventricular injection immediately after middle cerebral artery was occluded. Administration of LXA(4) ME ameliorated neurological deficit, reduced infarct volume, attenuated histological damage, and decreased number of apoptotic neuron induced by ischemic insult. These neuroprotective effects of LXA(4) ME were associated with inhibition of neutrophil infiltration, lipid peroxidation, and astrocyte activation. In addition, LXA(4) ME also attenuated proinflammatory cytokines (TNF-alpha and IL-1beta) production. These data suggest that LXA(4) ME protects neuron against permanent cerebral ischemia by inhibiting inflammatory responses.
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http://dx.doi.org/10.1007/s12031-010-9355-8 | DOI Listing |
Brain Res Bull
January 2025
Department of Neurology, Shanghai Tenth People's Hospital Chongming Branch, 2866 Chongming Road, Shanghai 202157, China.
Background: This study aimed to clarify whether the neuroprotective effect of LXA4 is associated with the targeting of neutrophil extracellular traps (NETs) in ischemic stroke (IS).
Methods: The MCAO rat model was established to assess cerebral infarction, brain water content and neurological deficits. ELISA was employed to examine the activities of MPO, NE, MMP-9.
Mol Neurodegener
November 2024
Herbert Wertheim School of Optometry and Vision Science, University of California, Berkeley, CA, USA.
Background: The resident astrocyte-retinal ganglion cell (RGC) lipoxin circuit is impaired during retinal stress, which includes ocular hypertension-induced neuropathy. Lipoxin B produced by homeostatic astrocytes directly acts on RGCs to increase survival and function in ocular hypertension-induced neuropathy. RGC death in the retina and axonal degeneration in the optic nerve are driven by the complex interactions between microglia and macroglia.
View Article and Find Full Text PDFAnn Clin Transl Neurol
October 2024
Department of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Background: Neuromyelitis optica spectrum disorder (NMOSD) is an anti-aquaporin 4 (anti-AQP4) autoantibodies-mediated idiopathic inflammatory demyelinating disease of the central nervous system. While intravenous pulse methylprednisolone (IVMP) is the recommended initial treatment option for acute onset NMOSD, its therapeutic mechanism remains unclear. We hypothesized that IVMP would reduce the expression of pro-inflammatory factors and increase the resolution of inflammation in patients with NMOSD.
View Article and Find Full Text PDFActa Neuropathol Commun
April 2024
Herbert Wertheim School of Optometry and Vision Science, University of California Berkeley, Berkeley, CA, USA.
Glaucoma leads to vision loss due to retinal ganglion cell death. Astrocyte reactivity contributes to neurodegeneration. Our recent study found that lipoxin B (LXB), produced by retinal astrocytes, has direct neuroprotective actions on retinal ganglion cells.
View Article and Find Full Text PDFbioRxiv
October 2024
Herbert Wertheim School of Optometry and Vision Science, University of California, Berkeley, CA, United States.
Background: The resident astrocyte-retinal ganglion cell (RGC) lipoxin circuit is impaired during retinal stress, which includes ocular hypertension-induced neuropathy. Lipoxin B produced by homeostatic astrocytes directly acts on RGCs to increase survival and function in ocular hypertension-induced neuropathy. RGC death in the retina and axonal degeneration in the optic nerve are driven by the complex interactions between microglia and macroglia.
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