| Backround and PurposeCerebral vascular accident(CVA) has a high mortality and disability. Cerebral infarction disease is a common type of CVA. Except thrombolysis and thrombolysis, now , neuroprotection drugs have been regard as a hot spot. These neuroprotection drugs are concentrated in two types, one can rescue neur of penumbra, and the other can stimulate the proliferation migration and differentiation of the neural precursor cells.Depression is a potentially life-threatening disorder that affects hundreds of millions of people. The initial hypothesis onthe action of antidepressant drugs was based mainly on the primary effect of trycyclics and monoamine oxidase (MAO) inhibitors on monoamine transporters and MAOs, respectively (the so-called monoamine hypothesis. With the move of much attention to examining the effect of chronic rather than acute antidepressant treatments, there is increasing evidence suggesting the involvement of changes in protein phosphorylation and expression of several genes linked to the survival, protection, and repair of neurons, including those of hippocampus in actions of antidepressant drugs. With the profound on 5-serotonin, there was a great progress on the discovery of antidepressant drugs, some selective serotonin reuptake inhibitors (SSRI)have been used in the clinical extensively and effectly.Fluoxetine, as a SSRI, is a confirm and effective antidepressant drug. There are many studies on the effect of fluoxetine on post-stroke depression(PSD). Someone found that neurofunctional recovery was equal with the depression recovery, but the degree of neurofunctional recovery was not equal with the depression recovery. Someone had found fluoxetine could improve the neurological function rehabilitition of post-stroke nondepressed patients. All these found suggest there are some unknown mechanisms on the fluoxetine neuroprotect.Now the studies on fluoxetine are concentrated in therapy against depression. Though there were some investigation on fluoxetine against cerebral-ischemia damage, they were limited tothe clinical investigation. There was few report about fluoxetine against cerebral-ischemia damage on mammal. This paper is to study the neuroprotection of fluoxetine against the focal cerebral ischemia-reperfusion injury in rats and anoxia-reoxygenation injury of rat hippocamal neurons in culture in vitro, and to find the mechanisms of it' s neuroprotection.Methods:1.Sixty adult male mice were divived in 6 groups. Three group will be used as controls, in which, animals receive only stomach-pouing with saline. Treatment during the same period of drug treatment in other three groups, where animals will receive chronic stomach-pouing of fluoxetine (20mg/kg) for 20 days. Animal model of focal cerebral ischemia and reperfusion were made by thread. Zea Longa method was used to evaluate behavioral change and TTC staining was applied to show cerebral infarction at 3h ischemia alone and 3h ischemia combined with reperfusion of 6h and 24h.2. The content of BDNF in hippocampus and areo around ischemia in 6h of ischemia combined with reperfusion of 24h with the Elivision method of immunocytochemistry.3. Hippocampus neurons were divived into 4 groups, which cultured by anoxia-reoxygenation in vitro. The effect of fluoxetine against neurons apoptosis after anoxia-reoxygenationdamage was analysised by MTT reduction assay and LDH releasing assay.Results1. Zea Longa evaluation of groups prevented with f luoxetine and controled groups are 2. 00 + 0.67, 2.20 + 0.42, 2. 33 + 0. 71and 2. 10 + 0. 57, 2. 27?. 47, 3. 00?. 82 at 3h ischemia alone and 3h ischemia combined with reperfusion of 6h and 24h. Zea Longa evaluation showed no difference between the groups prevented with f luoxetine and the control groups except in the group of 24h reperfusion following 3h cerebral ischemia, p0. 05. Cerebral infarction volume in groups prevented with fluoxetine and control groups are 11.24 + 3.31, 12. 60?. 02, 11. 56 + 2.40 and 11.16?. 50, 11.90 + 5.39, 15. 18 3.23. Samely, cerebral infarc...
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