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Chinese Journal of Pathophysiology ; (12): 739-744,753, 2018.
Article in Chinese | WPRIM | ID: wpr-701189

ABSTRACT

AIM: To investigate whether oxytocin has neuroprotective effects on hippocampal CA 1 pyramidal neurons from neonatal rats exposed to hypoxic-ischemic brain injury and the underlying mechanisms.METHODS:An in vitro model of hypoxic-ischemic injury was used by exposing the brain slices to oxygen-glucose deprivation(OGD)solution. Acute dissociated brain slices(6~8 slices per rat)from 8 Sprague-Dawely rats of 7~10 d old were used.The slices were randomly divided into 4 groups: control group, OGD 20 min group, OGD 40 min group and OGD +oxytocin group.The effect of oxytocin on neuronal death was evaluated by TO-PRO-3 staining.Fresh brain slices from other 20 neonatal rats were divided into OGD group,OGD+oxytocin group,OGD+dVOT(oxytocin receptor antagonist)+oxytocin group,and OGD+bicucuclline(GABAAreceptor antagonist)+oxytocin group.The onset of anoxic depolarization in the hippocampal neurons treated with different drugs was recorded by whole-cell patch-clamp techniques.RESULTS: The results of TO-PRO-3 staining showed that neuronal deaths in hippocampal CA 1 area were increased over the prolonged OGD time.Oxyto-cin significantly reduced the hypoxic-ischemic deaths.Oxytocin dramatically prolonged the onset time of anoxic depolariza-tion after the application of OGD solution.Both dVOT and bicuculline blocked this effect.CONCLUSION: Oxytocin plays a neuroprotective role in neonatal rat hippocampal CA 1 pyramidal neurons by enhancing the inhibitory synaptic trans-mission via oxytocin receptors.Therefore,oxytocin is useful as a candidate for neuroprotective treatment after neonatal hy -poxic-ischemic brain injury.

2.
Journal of Central South University(Medical Sciences) ; (12): 110-114, 2008.
Article in Chinese | WPRIM | ID: wpr-814112

ABSTRACT

OBJECTIVE@#To construct hypoxia/radiation inducible promotor HRE1.Egr-1, and to observe its promotive effect on the expression of yCDglyTK gene in nasopharyngeal cancer HNE-1 cells and the anti-tumor effect of yCDglyTK and to lay an experimental foundation for further exploration of new gene-radio therapy of nasopharyngeal cancer.@*METHODS@#pcDNA3.1(-)HRE1.Egr-1.yCDglyTK was constructed by gene recombination technique. Stable yCDglyTK-expressing HNE-1 cells were generated by transfecting the recombinant plasmid into the target cells with liposome. The expression of yCDglyTK was detected by Western blot in 4 groups: a normoxia group, a radiation group, a hypoxia group, and a hypoxia and radiation group. The killing effect of 5-FC in different circumstances was determined by MTT.@*RESULTS@#The expression of yCDglyTK/5-FC gene in all the groups was significantly different(P<0.01),especially in the hypoxia and radiation group. The killing effect of 5-FC on HNE1 cells varied under different conditions, especially in the hypoxia and radiation group.@*CONCLUSION@#Hypoxia and radiation can induce the activity of fusion promoter HRE1.Egr-1, and obviously promote the anti-tumor effect of yCDglyTK/5-FC system, suggesting that yCDglyTK may be a candidate suicide gene for gene-radio therapy of NPC.


Subject(s)
Humans , Early Growth Response Protein 1 , Genetics , Flucytosine , Pharmacology , Gene Fusion , Physiology , Genetic Therapy , Methods , Hypoxia-Inducible Factor 1, alpha Subunit , Genetics , Nasopharyngeal Neoplasms , Genetics , Radiotherapy , Therapeutics , Response Elements , Genetics , Thymidine Kinase , Genetics , Metabolism , Tumor Cells, Cultured
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