【摘要】 目的探讨氟西汀对大鼠缺血后再灌注海马的影响及可能机制。方法将40只Wistar大鼠随机等分成4组:①单纯用药组(氟西汀灌胃20 d);②正常对照组(氯化钠灌胃20 d);③术前用药组(氟西汀灌胃20 d制作脑缺血再灌注模型);④单纯手术组(氯化钠灌胃20 d制作脑缺血再灌注模型)。于实验终点进行苏木精-伊红染色及免疫组化检查,检测bcl-2和脑源性神经营养因子(BDNF)表达情况。结果与正常对照组比较,单纯用药组bcl-2检测指标无显著性差异(P>0.05),BDNF表达显著性增多(P<0.05)。术前用药组与单纯手术组比较,bcl-2表达无显著性差异(P>0.05),BDNF表达显著性增高(P<0.05)。结论氟西汀可以诱导增加BDNF表达,但不增加bcl-2的表达,从而减轻缺血后的再灌注损伤,产生神经保护作用。更多还原

【Abstract】 Objective To probe the effect of fluoxetine pretreatment on the hippocampus with ischemia-reperfusion injury and possible mechanism. Methods Forty Wistar rats were randomly divided into 4 groups of 10 each: medication-alone group that received fluoxetine by gastric gavage for 20 days; control group that received chloride solution by gastric gavage for 20 days; preoperative medication group, in which cerebral ischemia-reperfusion model was made after fluoxetine was infused into stomach for 20 days; simple operation group, in which cerebral ischemia-reperfusion model was made after sodium chloride solution was infused into stomach for 20 days. Then the expressions of bcl-2 and brain-derived neurotrophic factor (BDNF) were detected by immunohistochemical method and HE staining results were observed in all the groups. Results Compared with the control group, medication-alone group showed no significant difference in bcl-2 expression (P > 0.05), but had a significantlyhigher expression ofBDNF(P < 0.05). Compared with the simple operation group, the preoperative medication group showed no significant difference in bcl-2 expression (P > 0.05), but had a significantly higher expression of BDNF (P < 0.05). Conclusion Fluoxetine could induce a high-level BDNF expression with no increase of bcl-2 expression, thus relieving the cerebral ischemia-reperfusion injury and producingneuroprotection.更多还原