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目的阐明不同鼠龄在慢性间断性缺氧相关认知损害中的作用及可能机制。方法采用改良的IH鼠箱建立慢性IH小鼠模型,利用Morris水迷宫检测青年和老年IH小鼠的认知功能;通过氧疗的干预对比青年与老年小鼠认知损害及突触可塑性的改善程度,TUNEL法检测小鼠海马CA1区神经元凋亡情况,Western Blotting检测神经突触素、胰岛素信号通路蛋白[蛋白激酶B(Akt)、糖原合成激酶3β(GSK-3β)]的磷酸化表达水平变化。结果老年小鼠IH组的逃避潜伏期最长,其海马CA1区见明显增多的TUNEL染色阳性细胞,脑细胞凋亡率最高(P<0.01),p-Akt、p-GSK3β表达水平显著降低(P<0.01),目标象限LD滞留时间与p-Akt、p-GSK3β均存在正相关。结论老年使慢性间断性缺氧C57BL/6小鼠认知损害的易感性增加,可能的机制之一是调节胰岛素信号通路相关蛋白的表达异常。
Objective To elucidate the role and possible mechanism of different age in chronic cognitive impairment associated with chronic hypoxia. Methods Acute IH mouse model was established with an improved IH rat. Morris water maze was used to detect the cognitive function of young and old IH mice. The oxygen therapy intervention was used to compare the cognitive impairment and synaptic plasticity in young and old mice The levels of neuronal synaptophysin, phosphorylation of insulin signaling pathway protein [protein kinase B (Akt) and glycogen synthase kinase 3β (GSK-3β)] were detected by TUNEL assay. Changes in expression levels. Results The escape latency of IH group was the longest in hippocampus. TUNEL positive cells in hippocampal CA1 area were significantly increased (P <0.01), and the expression of p-Akt and p-GSK3β in P <0.01). There was a positive correlation between LD retention time and p-Akt and p-GSK3β in the target quadrant. Conclusion The elderly may increase the susceptibility to cognitive impairment in chronic intermittent hypoxic C57BL / 6 mice. One of the possible mechanisms may be the abnormal expression of related proteins in insulin signaling pathway.