Activation of Signal-Regulated Kinase 1/2 Exhibits Protective Effect on Neuronal Injury

In acute cerebral ischemia, activation of extracellular signal-regulated kinase 1/2 has been demonstrated.

Yaning Zhao and her colleagues, Hebei United University, China induced transient whole-brain ischemia by four-vessel occlusion in normal and diabetic rats and intravenously injected diabetic rats with extracellular signal-regulated kinase 1/2 30 minutes before ischemia as a pretreatment.

After Chronic Cerebral Ischemia, 3-N-Butylphthalide Improves Neuronal Morphology
The pathogenesis of vascular dementia induced by chronic cerebral ischemia is complex, mainly consisting of oxidative stress injury, energy metabolism disorder, cholinergic nerve dysfunction and neuronal apoptotic cell death.

Results showed that during the pathological progression of cerebral ischemia/reperfusion in rats, activation of extracellular signal-regulated kinase 1/2 exhibits protective effect on neuronal injury.

Reduced extracellular signal-regulated kinase 1/2 decreases Ku70 activity, increases Bax expression and thereby increases the number of lost hippocampal neurons in diabetic rats after cerebral ischemia/reperfusion. These results were published in Neural Regeneration Research (Vol. 9, No. 7, 2014).

Source-Eurekalert

Treating Cerebral Ischemia
For treating cerebral ischemia/reperfusion, mesenchymal stem cell transplantation is a novel means and can promote angiogenesis and neurological functional recovery.

Tau Protein Phosphorylation in Rats Subjected to Cerebral Ischemia-reperfusion Injury
Hyperphosphorylation of the microtu-bule-associated protein tau induced by transient brain ischemia, shows a study.

Research Explores Use of Salvianolate for Treatment of Cerebral Ischemia-Reperfusion Injuries
Previous research has shown that salvianolic acid B is a phenolic acid compound composed of three Danshensu units and one molecule of caffeic acid.