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目的采用非转基因的早老小鼠(senescence-accelerated prone mice,SAMP8)模型以观察隔离应激是否影响该模型小鼠脑内Amyloid-β(Aβ)水平及记忆功能。方法将SAMP8小鼠从断奶开始单独隔离饲养至6个月,空白对照组每3只一笼不给予隔离处理。于实验第3个月和6个月,采用条件恐惧实验、空间逆向学习法测定小鼠的学习记忆能力。行为学检测结束后,检测血浆皮质酮水平、测定海马体积、脑组织Aβ含量、观察Aβ斑块及蛋白羰基水平。结果 3个月时,应激小鼠关联和暗示记忆能力严重受损;6个月时,应激小鼠空间逆向学习能力下降明显。与空白对照组小鼠相比,血浆皮质酮水平在应激小鼠组明显升高,海马体积显著缩小。然而,隔离应激6个月后并不能明显增加脑组织内可溶性Aβ水平,也无Aβ斑块沉积,但脑组织蛋白羰基水平显著提高。结论隔离应激可加速SAMP8小鼠记忆功能减退,可能与脑内氧化应激损伤相关。
Objective To investigate the effects of isolated stress on the level of Amyloid-β (Aβ) and the memory function in non-transgenic mice with senescence-accelerated mice (SAMP8). Methods SAMP8 mice were isolated and reared individually for 6 months from the start of weaning. The blank control group was not given isolation treatment every 3 cages. At the third month and the sixth month of the experiment, the conditions of fear and space learning were used to determine the learning and memory abilities of mice. After behavioral testing, plasma corticosterone levels were measured, hippocampal volume, brain Aβ content and Aβ plaque and protein carbonyl levels were observed. Results At 3 months, the stress mice were implicated and implicated in impaired memory. At 6 months, the spatial learning ability of stress mice decreased significantly. Compared with the blank control group, the level of plasma corticosterone in the stress group was significantly increased, the volume of the hippocampus was significantly reduced. However, isolated stress did not significantly increase the level of soluble Aβ and no Aβ plaque in brain tissue after 6 months, but the protein carbonyl levels in brain tissue increased significantly. Conclusion Isolated stress can accelerate the memory deficit in SAMP8 mice, which may be related to oxidative stress injury in brain.