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目的:研究玉郎伞多糖(YLSP)对快速老化模型小鼠(SAMP8)额叶、海马神经元丢失和Tau(Ser202)异常磷酸化的影响。方法:选择6月龄SAMP8,随机分为模型组,石杉碱甲组(0.02 mg.kg-1),YLSP低、高剂量组(45,180 mg.kg-1),选择6月龄正常老化小鼠(SAMR1)作为对照组,以上各组每日上午灌胃给药l次,连续40 d,于末次给药的次日采用尼氏染色方法检测额叶和海马神经元缺失率;应用免疫组织化学方法检测额叶和海马Tau(Ser202)磷酸化水平。结果:模型组额叶、海马神经元缺失率分别为(46.4±8.4)%,(45.5±7.2)%。与模型组相比,石杉碱甲组(35.8±6.7)%,(34.2±5.6)%、YLSP低、高剂量组(35.1±6.4)%,(36.0±4.5)%,(25.6±6.6)%,(26.7±6.1)%额叶、海马神经元缺失率明显降低(P<0.05或P<0.01);模型组额叶、海马pSer202阳性细胞数(92.2±10.7),(98.6±11.4)个较对照组明显升高(12.3±2.1),(15.5±2.6)个(P<0.01),与模型组相比,石杉碱甲组(48.5±6.4),(56.1±3.3)个、YLSP低、高剂量组(60.7±7.5),(65.9±8.0);(50.9±5.1),(53.6±6.7)个的额叶、海马Tau(pSer202)阳性细胞数明显降低(P<0.01)。结论:YLSP降低Tau蛋白异常磷酸化,减少脑部神经元缺失。
Objective: To investigate the effects of YLSP on the frontal lobe and hippocampal neurons loss and the abnormal phosphorylation of Tau (Ser202) in senescence accelerated mouse (SAMP8). Methods: Six-month-old SAMP8 were randomly divided into model group, huperzine A group (0.02 mg.kg-1), low YLSP and high dose group (45,180 mg.kg-1) (SAMR1) served as control group. The above groups were orally administered once a day for 40 consecutive days, and the missing rate of frontal lobe and hippocampus neurons was detected by Nissl staining on the next day after the last administration. Immunohistochemistry The chemical method was used to detect phosphorylation of Tau (Ser202) in frontal lobe and hippocampus. Results: The loss rate of frontal lobe and hippocampus neurons in the model group were (46.4 ± 8.4)% and (45.5 ± 7.2)%, respectively. (35.8 ± 6.7)%, (34.2 ± 5.6)%, low YLSP, high dose group (35.1 ± 6.4)%, (36.0 ± 4.5)% and (25.6 ± 6.6) %, (26.7 ± 6.1)% of the frontal lobe and hippocampus significantly decreased (P <0.05 or P <0.01). The positive cells of pSer202 in the frontal lobe and hippocampus in the model group were 92.2 ± 10.7 and 98.6 ± 11.4 (12.3 ± 2.1) and (15.5 ± 2.6), respectively (P <0.01). Compared with the model group, the huperzine A group (48.5 ± 6.4), (56.1 ± 3.3), the low YLSP , High dose group (60.7 ± 7.5), (65.9 ± 8.0); (50.9 ± 5.1), (53.6 ± 6.7) frontal lobe, hippocampus Tau (pSer202) positive cells decreased significantly (P <0.01). Conclusion: YLSP can reduce the abnormal phosphorylation of Tau protein and reduce the loss of neurons in the brain.