sodium-dodecyl-sulfate has been researched along with Infarction--Middle-Cerebral-Artery* in 1 studies
1 other study(ies) available for sodium-dodecyl-sulfate and Infarction--Middle-Cerebral-Artery
Article | Year |
---|---|
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
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 |