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目的评估灵芝制剂对APP/PS1双转基因阿尔茨海默病(AD)小鼠行为学、生物化学和自身免疫指标的影响。方法将44只4月龄APP/PS-1双转基因AD小鼠随机分为AD模型组、安理申组、灵芝中剂量组和灵芝高剂量组4组,每组11只,以10只4月龄C57BL/6小鼠为对照组。水迷宫实验观测小鼠的行为学变化情况,Western blot法检测脑组织蛋白表达水平,间接免疫荧光法检测自身免疫指标。结果定位航行实验结果显示,从第2天起,对照组、灵芝高剂量组和中剂量组寻找平台时间呈现逐渐缩短趋势,AD模型组寻找平台时间呈现逐渐增加趋势;第5天,对照组(t=5.607,P=0.000)和灵芝高剂量组(t=2.750,P=0.010)寻找平台时间较模型组明显缩短。空间探索实验结果显示,AD模型组小鼠穿越目标平台所在象限的次数(t=2.452,P=0.025)和在目标象限内滞留时间(t=2.530,P=0.020)明显少于对照组小鼠,穿越目标平台次数较灵芝组高剂量组(t=2.317,P=0.030)和灵芝中剂量组明显减少(t=2.443,P=0.030),且目标象限停留时间较灵芝高剂量组明显减少(t=2.770,P=0.020);灵芝高剂量组小鼠穿越目标平台所在象限的次数(t=2.493,P=0.022)和在目标象限内滞留时间(t=2.683,P=0.015)明显多于安理申组小鼠。Western blot检测结果显示,灵芝高、中剂量组小鼠脑组织中Apo A1表达水平显著高于AD模型组(P<0.01,P<0.05);灵芝高剂量组Aβ-40表达水平显著低于AD模型组(P均<0.05);灵芝高剂量组小鼠脑组织中的Sty1、Apo E、ABCA1水平显著高于模型组(P<0.01,P<0.05)。安理申组(t=30.945,P=0.000)、灵芝中剂量组(t=25.639,P=0.000)和灵芝高剂量组(t=4.689,P=0.001)的血浆Ig G水平明显高于对照组。结论灵芝制剂可能改善AD小鼠行为学障碍,促进Apo A1、Apo E和Syt1的表达,抑制Aβ-40蛋白的表达,改善小鼠的自身免疫功能。
Objective To evaluate the effects of Ganoderma lucidum on behavioral, biochemical and autoimmunity in APP / PS1 double transgenic Alzheimer’s disease (AD) mice. Methods Forty-four 4-month-old APP / PS-1 double transgenic AD mice were randomly divided into four groups: AD model group, Amikasone group, Ganoderma lucidum medium dose group and Ganoderma lucidum high dose group, with 11 rats in each group. C57BL / 6 mice as control group. Morphological changes of mice were observed by water maze test, protein expression of brain tissue was detected by Western blot and indirect immunofluorescence method was used to detect autoimmunity index. Results The navigation experiment results showed that from the second day onward, the searching time of the control group, Ganoderma lucidum high-dose group and middle-dose group showed a trend of shortening gradually, and the time of looking for the platform of AD model group showed a gradual increasing trend. On the fifth day, t = 5.607, P = 0.000) and Ganoderma lucidum high dose group (t = 2.750, P = 0.010). The results of spatial exploration experiments showed that the number of mice crossing the target platform in the AD model group (t = 2.452, P = 0.025) and in the target quadrant (t = 2.530, P = 0.020) (T = 2.443, P = 0.030), and the target quadrant dwell time was significantly lower than that of the high-dose Ganoderma lucidum group (t = 2.317, P = 0.030) t = 2.770, P = 0.020). The number of mice in high-dose Ganoderma lucidum group crossing the target platform was significantly higher than that in the target quadrant (t = 2.493, P = 0.022) Allison group mice. The results of Western blot showed that the expression level of Apo A1 in brain of high and medium dose Ganoderma lucidum group was significantly higher than that of AD model group (P <0.01, P <0.05); the expression level of Aβ-40 in Ganoderma lucidum high dose group was significantly lower than that of AD model group (P <0.05). The levels of Sty1, Apo E and ABCA1 in brain of high-dose Ganoderma lucidum group were significantly higher than those in model group (P <0.01, P <0.05). The levels of plasma IgG in Angstrom group (t = 30.945, P = 0.000), Ganoderma lucidum middle dose group (t = 25.639, P = 0.000) and Ganoderma lucidum high dose group (t = 4.689, P = 0.001) were significantly higher than those in control group . Conclusion Ganoderma lucidum preparation may improve the behavioral disorders of AD mice, promote the expression of Apo A1, Apo E and Syt1, inhibit the expression of Aβ-40 protein and improve the autoimmune function in mice.