sodium-dodecyl-sulfate and Infarction--Middle-Cerebral-Artery

sodium-dodecyl-sulfate has been researched along with Infarction--Middle-Cerebral-Artery* in 1 studies

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1 other study(ies) available for sodium-dodecyl-sulfate and Infarction--Middle-Cerebral-Artery

ArticleYear
Lithium upregulates growth-associated protein-43 (GAP-43) and postsynaptic density-95 (PSD-95) in cultured neurons exposed to oxygen-glucose deprivation and improves electrophysiological outcomes in rats subjected to transient focal cerebral ischemia foll
    Neurological research, 2022, Volume: 44, Issue:10

    Lithium has numerous neuroplastic and neuroprotective effects in patients with stroke. Here, we evaluated whether delayed and short-term lithium treatment reduces brain infarction volume and improves electrophysiological and neurobehavioral outcomes following long-term recovery after cerebral ischemia and the possible contributions of lithium-mediated mechanisms of neuroplasticity.. Male Sprague Dawley rats were subjected to right middle cerebral artery occlusion for 90 min, followed by 28 days of recovery. Lithium chloride (1 mEq/kg) or vehicle was administered via intraperitoneal infusion once per day at 24 h after reperfusion onset. Neurobehavioral outcomes and somatosensory evoked potentials (SSEPs) were examined before and 28 days after ischemia-reperfusion. Brain infarction was assessed using Nissl staining. Primary cortical neuron cultures were exposed to oxygen-glucose deprivation (OGD) and treated with 2 or 20 μM lithium for 24 or 48 h; subsequent brain-derived neurotrophic factor (BDNF), growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD-95), and synaptosomal-associated protein-25 (SNAP-25) levels were analyzed using western blotting.. Compared to controls, lithium significantly reduced infarction volume in the ischemic brain and improved electrophysiological and neurobehavioral outcomes at 28 days post-insult. In cultured cortical neurons, BDNF, GAP-43, and PSD-95 expression were enhanced by 24- and 48-h treatment with lithium after OGD.. Lithium upregulates BDNF, GAP-43, and PSD-95, which partly accounts for its improvement of neuroplasticity and provision of long-term neuroprotection in the ischemic brain.

    Topics: Animals; Brain Ischemia; Brain-Derived Neurotrophic Factor; Disks Large Homolog 4 Protein; Edetic Acid; GAP-43 Protein; Glucose; Glycogen Synthase Kinase 3 beta; Infarction, Middle Cerebral Artery; Lithium; Lithium Chloride; Male; N-Methylaspartate; Neurons; Neuroprotective Agents; Oxygen; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Sodium Dodecyl Sulfate

2022