氯胺酮通过改变Fos和Bcl-2表达减轻缺氧对大鼠海马群峰电位的抑制

发布时间：2018-05-02 05:03

本文选题：氯胺酮 + 大鼠海马神经元　；参考：《华中科技大学学报(医学版)》2017年05期

【摘要】：目的通过观察氯胺酮处理对缺氧引起的大鼠海马诱发群峰电位、神经元Fos、Bcl-2表达的影响,探讨氯胺酮对神经元缺氧性损伤保护作用机制。方法脑片以及培养细胞随机分为3组:对照组(不进行缺氧处理)、缺氧组和氯胺酮组(缺氧前于培养液中加入氯胺酮,终浓度为20μmol/L,其它处理同缺氧组)。脑片记录:成年雄性Wistar大鼠麻醉后取海马切片,进行CA3区Schaffer侧支刺激,记录CA1区椎体细胞诱发电位。新生大鼠海马神经元培养7~11d,分组处理后进行免疫组化染色,计算Fos、Bcl-2阳性细胞率。结果氯胺酮预处理后,海马脑片群峰电位开始减小和完全消失的时间延迟;培养海马神经细胞Fos表达阳性率、平均吸光度值与缺氧组比较明显减少(均P0.05);海马神经细胞Bcl-2表达阳性率、平均吸光度值与缺氧组比较明显增加(均P0.05)。结论氯胺酮预处理对大鼠海马群峰电位的保护作用可能是通过减少缺氧后Fos表达、增加Bcl-2表达来实现的。
[Abstract]:Objective to observe the effects of ketamine treatment on hippocampal evoked group potential and expression of Foschelin-Bcl-2 in rat hippocampal neurons induced by hypoxia, and to explore the protective mechanism of ketamine on hypoxic neuronal injury. Methods brain slices and cultured cells were randomly divided into three groups: control group (control group), anoxic group and ketamine group (Ketamine was added to the culture medium before hypoxia and the final concentration was 20 渭 mol / L). Brain slice recording: adult male Wistar rats were anesthetized and the hippocampal slices were taken and stimulated with the lateral branches of Schaffer in the CA3 area. The vertebral cell evoked potentials in the CA1 area were recorded. The hippocampal neurons of neonatal rats were cultured for 7 ~ 11 days and then treated with immunohistochemical staining to calculate the rate of Fosson-Bcl-2 positive cells. Results after Ketamine preconditioning, the peak potentials of hippocampal slices began to decrease and disappeared completely, and the positive rate of Fos expression in cultured hippocampal neurons was increased. Compared with hypoxia group, the average absorbance value decreased significantly (P 0.05), and the positive rate of Bcl-2 expression in hippocampal nerve cells was significantly higher than that in hypoxia group (all P 0.05). Conclusion the protective effect of ketamine preconditioning on hippocampal group peak potential in rats may be achieved by reducing the expression of Fos and increasing the expression of Bcl-2 after hypoxia.
【作者单位】：华中科技大学同济医学院附属同济医院麻醉学教研室;武汉市第三医院麻醉科;华中科技大学同济医学院附属协和医院神经内科;
【基金】：国家自然科学基金资助项目(No.81371251)
【分类号】：R614

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