Preconditioning and post-treatment with cobalt chloride in rat model of perinatal hypoxic–ischemic encephalopathy

摘要: Abstract Background: Hypoxia–ischemia (HI)-induced perinatal encephalopathy is a major cause of acute mortality and chronic neurologic morbidities such as cerebral palsy, mental retardation, epilepsy. As the essential transcription factor for activation hypoxia-inducible genes, 1 alpha (HIF-1α) plays an important role in pathophysiological response to stress HI brain damage. Whether HIF-1α promotes neuroprotection tissues controversial. Methods: The left common carotid artery rats aged 7days was ligated under anesthesia. pups were then exposed hypoxia normobaric chamber filled with 8% oxygen 92% nitrogen 2.5h. In sham control group, but not or hypoxia. To assess time window effective treatment, inducer cobalt chloride (CoCl 2 ) injected subcutaneously 1day before surgery, immediately after surgery. harvested from each groups at 1, insult protein ant its target genes expression investigating injury. Morris water maze tests performed postnatal 7weeks. Results: levels vascular endothelial growth factor, heme oxygenase-1, insulin-like markedly increased intraperitoneal injection CoCl (60mg/kg). gene inducible nitric oxide synthase exhibited biphasic course. caused apoptosis reduced capillary density, which ameliorated by . Both preconditioning 24h administration improved long-term reference memory compared that vehicle-injected littermate controls. Administration did improve spatial working memory. Conclusions: activates protects against damage vivo. could be used manipulate activity pathways promote recovery.