| The expression of various neurotrophic factors (NTFs)and neuron growth (NGI) increase after cerebral ischemia, which is great important to restore and regenerate injured neurons. Brain-derived neurotrophic factor (BDNF) belongs to the family of nerve growth factor, that is neurotrophic factors. Experiments before confirmed that BDNF can stimulate and promote the survival of various neurons. BDNF also plays an important role on repairment of injured neurons after cerebral ischemia. The more serious cerebral ischemia occurs, the more obviously BDNF expresses. Traditional ideas are that central nerve system (CNS) is difficult to regenerate due to deficiency of NTFs. But large quantities of experiments demonstrate that, when CNS hurt, the regeneration of injured neurons isn't obvious simply provide with NTFs. It hints that there also exist neuron growth inhibitors in CNS. They are important of targeting of axons and regeneration of CNS. Semaphorin3A (Sema3A) is a kind of NGI, which can make growth cone collapse. The expression of Sema3A may increase after neurons injured. As a result, giving BDNF or Sema3A inhibitors, which may be a new way to resolve the repairment and regeneration of injured neurons, can repair the injured neurons. However, because BDNF and Sema3A are difficult to pass through blood-brain-barrier (BBB), the use is limited. Puerarin can dilate coronal vessels and cerebral vessels, and also can promote microcirculation. But it's influence on the expression of BDNF and Sema3A after cerebral ischemia is unkown before. In this study, we produced a model of cerebral ischemia, and observed the expression of BDNF and Sema3A after focal cerebral ischemia and the change after giving puerarin, to study it's neuroprotective function. Male Wistar rats weighted from 250g to 300g were randomly divided into four groups: normal control group, sham-operation group, ischemia group and treat group. According to ischemia time, ischemia group and treat group are divided respectively into 6 h, 1 d, 3 d, 5 d, 7 d, 14d sub-group. Ischemia group is given saline after MACO, while treat group is given puerarin (0.1mg/kg/d) after MACO. The model of focal cerebral ischemia was set up by MACO. Dynamic changes of BDNF and Sema3A positive neurons number at different time were observed with method of immunohistochemistry, and the picture analysis was applied. The results in normal control group and sham-operation group revealed that BDNF and Sema3A positive neurons numbers were low level. There were no significant different between the two groups (P>0.05). In ischemia group and treat group, BDNF and Sema3A positive neurons numbers increased obviously after 6 hours of MACO, and reached high peak at one day after MACO. In ischemia group, the above increases of BDNF and Sema3A positive neurons numbers were no longer observed after 3 days of MACO. The BDNF positive neurons number in treat group was higher than that in ischemia group (P<0.05). In contrast, the Sema3A positive neurons number in treat group was lower than that in ischemia group (P<0.05). These findings suggest that the temporal endogenetic up-regulation of BDNF positive neurons number after MACO may be related to the mechanism of neuronic injury and repairment. However, the temporal endogenetic up-regulation of BDNF positive neurons number is low, which is deficient to prevent and cure neuronic death. Moreover, BDNF is difficult to pass through BBB, thus, it's use is limited. Therefore, to explore a way of promoting endogenetic expression of BDNF is especially important. In this study, we found that the BDNF positive neurons number increased after giving puerarin, which suggests that puerarin, a micromolecular drug, can pass through BBB, and have neuroprotective effects by promoting the expression of BDNF. At the same time, the results of up-regulation of Sema3A positive neurons number after MACO suggest that foreign factors, eg. cerebral ischemia, may induce the up-regulation. It implied that Sema3A may inhibit the regenerati...
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