Hypoxia-inducible Factor 1¦Á, And Inducible Nitric Oxide Synthase In Neural Stem Cells To Hypoxia, Reoxygenation Injury In Rats

Objective: Discussion the Hypoxia inducible factor1α(HIF-1α) and Nducible nitric oxide synthase (iNOS) on the neural stem cells of oxygen reoxygenation injury relations.Methods: Health and removed within 24 hours of the Wistar rats sterile conditions removed brain, stripping meninges, the separation hippocampus, Hank's liquid rinse, moved to the pre-accession adequate basis for the culture medium (DMEM/F12) in the vial, scissors Broken, wind and percussion into a cell suspension, filtered mass, density is raised to 5×105/ml after training into 25 ml bottle culture. 7-8 d passage once. Kit provided by the method of nestin staining. The experimental group will be divided into two groups (Group hypoxia and hypoxia - oxygen-the two groups) to final concentration of 150 uM-CoCl2 medium cultured cells, hypoxia of simulation model. Hypoxia 4 h after removal of CoCl2 a complex model of oxygen (group). Determination of the two groups NSCs proliferation; RT-PCR test of HIF-1αmRNA, iNOS mRNA level; DNA fragment Determination of the NSCs apoptosis.Results: With the extension of hypoxia, HIF-1αmRNA expression increased in hypoxic and peaked at 8 hours;iNOS mRNA expression increased in hypoxic 12 hours at peak level. Reoxygenation HIF-1αmRNA and iNOS mRNA expression were reduced. HIF-1αmRNA expression of iNOS mRNA rate than large. Hypoxic 8 hours apoptosis and the normal control group had no significant change, 12 hours after hypoxia apoptosis significantly increased.Conclusion: HIF-1αmRNA and iNOS mRNA expression increased neural stem cells can promote the proliferation of neural stem cells inhibit apoptosis. HIF-1αsignificantly in the role of iNOS.