论文部分内容阅读
目的探讨成年大鼠单侧海马CA1区毁损后,海马齿状回(DG)神经发生新生细胞存活与自噬的关系。方法建立海人酸(KA)损毁单侧海马的模型,用5-溴脱氧尿嘧啶核苷(BrdU)于毁损后3d标记增殖的细胞,免疫组织化学检测BrdU阳性细胞,采用体视学的计数方法计算DG的BrdU阳性细胞总数。用自噬特异性抗原微管相关蛋白轻链3(LC-3)与BrdU双标的方法检测这些新生细胞的减少是否有自噬的参与。结果假毁损组DG区可见少量的BrdU阳性细胞;与假毁损组比较,实验组在海马毁损后DG区BrdU阳性细胞明显增加,差异有统计学意义(P<0.05),在BrdU给药后第1天最多,随着时间的推移逐渐减少,各组之间差异有统计学意义(P<0.05);各时间点均未见BrdU和LC-3双标细胞。结论成年大鼠海马毁损可增强DG的神经发生,新生细胞随着时间的推移逐渐减少,而自噬性程序性细胞死亡在新生细胞减少的调控中可能不占主导作用。
Objective To investigate the relationship between autophagy and neovascularization of hippocampal dentate gyrus (DG) neurons in adult rat hippocampal CA1 region. Methods The model of unilateral hippocampal CA1 damage was established by kainate (KA). The proliferated cells were labeled with BrdU for 3 days and the BrdU positive cells were detected by immunohistochemistry. Methods Calculate the total number of BrdU positive cells in DG. The autophagy-specific antigen microtubule-associated protein light chain 3 (LC-3) and BrdU double labeling method to detect whether these newborn cells reduce the autophagy. Results BrdU-positive cells were observed in the DG area of the sham-damaged group. Compared with the sham-damaged group, the number of BrdU positive cells in the DG area of the experimental group was significantly increased after the hippocampus was destroyed (P <0.05) The number of BrdU and LC-3 double-labeled cells in each group was no significant difference at each time point (P <0.05). Conclusion The damage of hippocampus in adult rats can increase the neurogenesis of DG. The number of neonatal cells decreases gradually with the passage of time. However, apoptosis of autophagic cells may not play a dominant role in the regulation of neovascular cells.