| Today in most countries ischemic stroke does harm to people' s health seriously. It becomes a hot topic to study the pathophysiologic mechanisms of ischemic stroke and search for efficient way to thera-peut it. Following the study carrying out , some people has pointed out that there is a rim of mild to moderately ischemic tissues ( ische-mic penumbra ) between the normal perfused brain and the evoking infarct. Its size varies according to the time and the therapy. The the-ory of ischemia - reperfusion injury contains four reactive mecha-nisms: excitotoxic injury and perrinfarct deplarization and inflamma-tion and apoptosis as well. The cascade of damage takes place mainly in the ischemic penumbra.In the course of these studies, many people pay attention to Brain -Derived Neurotrophic Factor( BDNF ) with multifunction, which is associated with lots of physiologic and pathophysiologic processes in bodies.Many studies suggested that BDNF can limit the cascade of dam-age following brain ischemia, up to now, people have studied the ex-pression of BDNF mRNA in MCAO models. But the results did not a-gree with each other.In our experiment we studied the expression of BDNF protein inMCAO rat model and discussed the protective machenisms.Material and MethodThere are 30 male Wistar rats, and they weight 280 - 320g re-spectively. They were divided randomly into three groups. Normal control group: three rats, sham - operated group three rats, ischemic - reperfusion group: twenty ?four rats, they were further divided into eight subgroups evenly at different time point such as 15min, 30min, 1h, 2h, 4h, 6h, 12h, 24h reperfused after suffering ischemia ninety minutes. The rats in ischemia - reperfusion group were operated ac-cording to the improved MCAO. The rats in sham - operation were op-erated as the rats in ischemia - reperfusion, except of not pulling the mononalon line into the EGA. Rats in normal control group were not operated at all.The brain was divided into five portions evenelly. The third chop were fixed. The method of SP immunostaining was used to study the expression of BDNF protein.ResultOnly a few neurons in the cerebral cortex show a weak labeling after staining with BDNF antiserum in normal controls and sham ?ope rated controls. In MCAO Group: the most marked up -regulation oc-cus in neurons with the infarcts and the border zone . Neurons in the border zones showed a moderately intense expression. Signs of BDNF up - regulation also seemed to occur in the contralateral hemisphere. 15 min after reperfusion, a diffuse expression of BDNF was found, which further intensified until Ih. The peak levels of BDNF were found 2h. Beginning to decline at 4h. The levels of BDNF hadreached control level at 24h.DisscussionIn our study immunohistochemical findings demonstrated that only a few neurons show a weak labeling after staining with BDNF antise-rum in normal controls and sham - operated controls. BDNF was in-creased in infarct or penumbra ( especially in the border zones) versus normal contralateral hemisphere. It suggests that few BDNF expression in normal brain tissues and that operation dont have effect on BDNF expression. BDNF expression up - regulates evidently following suffer-ing from hypoxia - ischemia stimulation. It demonstrated that BDNF protein is related to the pathphysiologic processes after the hypoxia -ischemia injury. An explanation for the high levels of BDNF in the pe-numbra might be that hypoxia ?induced stress of neurons increase BDNF expression. If the stress is too severe, cells might not respond as efficiently (lower levels observed in infarcts). We found that the most immunochemical staining positive cells are neurons. The fact suggests that BDNF mainly derives from neurons.Hypoxia - ischemia injury induced a great deal of excitotoxicity glutamate. Inappropriate activation of glutamate receptors is thought to be responsible for the death of neurons following brain insults such as ischemia. It is widely believed that the deleterious effect...
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