高血糖影响海马GSK3β-β-catenin信号抑制大鼠海马颗粒下区成体神经干细胞再生

发布时间：2018-04-17 20:12

本文选题：型糖尿病 + 神经干细胞　；参考：《神经解剖学杂志》2017年04期

【摘要】：目的:探讨持续高血糖对大鼠海马颗粒下区(subgranular zone,SGZ)神经干细胞状态的影响及可能机制。方法:SD大鼠注射链脲佐菌素(streptozotocin,STZ)诱导1型糖尿病模型,腹腔注射5-溴脱氧尿嘧啶核苷(bromodeoxyuridine,Brd U)标记新生细胞。利用免疫组化法检测海马SGZ区Ki67,5-溴脱氧尿嘧啶核/双皮质素(bromodeoxyuridine/doublecortin,Brd U/DCX)标记的阳性细胞。利用免疫印迹法检测海马胰岛素受体β(insulin receptorβ,IRβ),糖元合成酶激酶3β(pho-glycogen synthase kinase-3β,GSK3β),β-链蛋白(β-Catenin)表达水平。结果:STZ注射大鼠胰岛素降低,血糖升高;糖尿病大鼠海马区Ki67阳性细胞,Brd U/DCX阳性细胞和对照组比较明显减少,海马区IRβ,pho-GSK3β,β-Catenin表达水平和对照组比较显著下降(P0.05)。结论:STZ诱导的1型糖尿病大鼠海马SGZ区新生细胞增值能力下降,细胞分化异常,这一变化和海马区胰岛素信号下调,GSK3β活化,β-Catenin降解增加有关。
[Abstract]:Aim: to investigate the effect of hyperglycemia on the status of neural stem cells (NSCs) in the subgranular area of rat hippocampus and its possible mechanism.Methods the rat model of type 1 diabetes was induced by injection of streptozotocin (STZ) into the rat with 5 bromodeoxyuridine (Brd) labeled with 5-bromodeoxyuridine (Brd).The immunocytochemical method was used to detect the positive cells labeled with bromodeoxyuridine r-doublecortinus Brd U / DCX in the Ki67 ~ 5- bromodeoxyuridine (BDP) -bromodeoxyuridine r-doublecortinus (Brd / DX) in the hippocampal SGZ region.The expression levels of insulin receptor 尾 insulin receptor 尾 -IR 尾, glycogen synthase 3 尾 -phospho-glycogen synthase kinase-3 尾 -GSK3 尾, 尾 -catenin in hippocampus were detected by Western blotting.Results compared with the control group, the levels of IR 尾 -GSK3 尾, 尾 -Catenin and IR 尾 -GSK3 尾, 尾 -Catenin in hippocampal area of diabetic rats were significantly decreased (P 0.05), while those of Ki67 positive cells in hippocampus of diabetic rats were significantly decreased as compared with those of control group.Conclusion in type 1 diabetic rats, the proliferative ability of newborn cells in the hippocampal SGZ region is decreased and the differentiation is abnormal, which is related to the down-regulation of GSK3 尾 activation and the increase of 尾 -Catenin degradation in the hippocampal insulin signal.
【作者单位】：兰州大学基础医学院人体解剖学与组织胚胎学暨神经科学研究所;兰州大学基础医学院生物化学与分子生物学研究所;
【基金】：国家自然科学基金(81370448) 兰州大学中央高校基本科研业务费(lzujbky-2015-159)
【分类号】：R587.2

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