Articles tagged with Brain Ischemia
Researchers found that hypothermia can limit cell death and dynamin levels in mice with cerebral blockage. This suggests that dynamin may be a potential drug target for stroke-related neuronal cell death.
Research suggests that autophagy may be both beneficial and detrimental to neuronal survival after stroke. The study proposes that autophagy has dual effects on neuronal survival, highlighting the need for further investigation into its therapeutic potential.
Research by Dr. Hyung-Seok Kim reveals that early expressions of hypoxia-inducible factor 1 alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous NSCs after focal cerebral ischemia. Additionally, neural precursor cells can be recruited from nearby areas to promote neurofunctional recovery.
Researchers found that 3-n-butylphthalide improved neuronal morphology in the cerebral cortex and hippocampus, reducing oxidative stress caused by chronic cerebral ischemia. The compound also inhibited amyloid beta accumulation and improved cholinergic function in rats with chronic cerebral ischemia.
Researchers studied rat and mouse models of focal cerebral ischemia to develop high-quality rodent models of stroke. They found optimal methods for middle cerebral artery occlusion in rats (0.40-0.45 mm, 18-20 mm thread insertion length) and mice (0.15-0.18 mm, 9-11 mm thread insertion length).
The Houshiheisan compound prescription effectively suppresses abnormal amyloid precursor protein accumulation and reduces amyloid substance deposition. It maintains the stabilization of the internal environment of neurovascular units, minimizing injury to these units in the ischemic penumbra.
Researchers found that transient brain ischemia induces hyperphosphorylation of tau protein and alters its interaction with glycogen synthase kinase (GSK)-3β and protein phosphatase 2A. Lithium chloride's neuroprotective function may depend on regulating tau phosphorylation during cerebral ischemia.
Researchers found that brain-derived neurotrophic factor suppressed glucose intolerance by improving insulin receptor expression and inhibiting gluconeogenesis in the liver. This suggests a potential therapeutic hypothesis for treating glucose intolerance after cerebral ischemia.
The study reveals rutaecarpine's ability to improve neurological function after cerebral ischemia reperfusion injury. The mechanism involves reducing oxidative stress, providing a promising basis for rutaecarpine as an ideal drug for preventing and treating cerebral ischemia reperfusion injury.
Research found that 60-minute sevoflurane preconditioning reduces infarct volume and apoptotic cells, but longer durations do not provide additional benefits. The study suggests that shorter preconditioning periods may be more effective in protecting against cerebral ischemia.
Researchers found that cilostazol decreases hypoxia-inducible factor-1α and heme oxygenase-1 expression levels, protecting against cognitive impairment induced by chronic cerebral ischemic injury. Cilostazol treatment also exhibits an anti-apoptotic mechanism in the context of chronic cerebral ischemia.
The motor relearning program significantly promotes neuronal regeneration and repair, as well as angiogenesis in damaged brain tissue. This study provides a new theoretical idea for the clinical treatment of brain ischemia.