牛磺酸对阿尔茨海默病模型大鼠学习记忆能力的影响

发布时间：2018-05-31 01:07

本文选题：牛磺酸 + β淀粉样肽　；参考：《青岛大学》2012年硕士论文

【摘要】：目的：研究牛磺酸对阿尔茨海默病(Alzheimer's disease,AD)大鼠学习记忆能力的影响。方法：雄性SD大鼠,随机分为正常组、假手术组、模型组、阳性治疗组、牛磺酸大、中、小剂量组。海马微量注射凝聚态β淀粉样肽1-40(β-amyloid peptide1-40, Aβ1-40)制作AD模型,阳性治疗组采用哈伯因灌胃治疗,牛磺酸大、中、小剂量组采用不同剂量(600、400、200mg·kg-1·d-1)牛磺酸灌胃治疗4周。用Morris水迷宫进行行为学测试,水迷宫测试完毕24h,大鼠断头取脑,测定海马和皮质中乙酰胆碱(Acetylcholine,Ach)、乙酰胆碱酯酶(Acetylcholine Esterase,Ache).乙酰胆碱转移酶(Choline Acetyltransterase,ChAT)、超氧化物歧化酶(Superoxide Dismutase,SOD)、丙二醛(Malondialdehyde,MDA).谷胱甘肽过氧化物酶(Glutathione Peroxidase,GSH-Px)的活性,大脑切片HE染色观察AD模型大鼠海马病理学改变。结果：Morris水迷宫实验,牛磺酸中、大剂量组逃避潜伏期均明显比模型组缩短[(39.08±5.23)(39.11±2.24)(43.21±3.46)s,P0.05]；牛磺酸中、大剂量组穿站台次数和第三象限游泳时间均比模型组明显延长[(4.38±1.06)(4.10±1.10)(2.89±1.69)P0.05],[(38.90±3.35)(38:92±3.31)(34.96±4.30)s,P0.05]。与模型组相比,牛磺酸中、大剂量组海马组织中Ach含量和ChAT活性均明显增加[(159.06±13.16)(160.10±9.88)(144.50±17.39)u g/ml,P0.05],[(225.36±22.30)(222.12±21.41)(201.67±33.80)IU/g,P0.05],Ache活性明显降低[(122.25±11.99)(120.45±11.20)(143.11±19.68)U/mgprot,P0.05]。牛磺酸中、大剂量组皮质组织中Ach含量和ChAT活性均明显增加[(160.31±12.64)(159.10±9.83)(143.39±18.70)u g/ml,P0.05],[(214.81±20.17)(216.06±27.13)(190.89±23.44)IU/g,P0.05],Ache活性明显降低[(118.88±12.43)(117.05±8.96)(139.37±11.81)U/mgprot,P0.05]；牛磺酸中、大剂量组海马组织中SOD、GSH-PX活性明显增加[(209.38±34.48) (209.33±29.67) (179.78±28.38) U·mg-1, P0.05], [ (35.71±7.66)(35.36±6.63) (28.77±8.12) U·g-1, P0.05], MDA含量明显降低[(1.93±0.32)(1.89 + 0.30) (2.38±0.52) nmol·mg-1, P0.05]。牛磺酸中、大剂量组皮质组织中SOD、GSH-PX活性明显增加[(199.38±31.22) (201.05 + 26.93 ) (172.00±16.46)U·mg-1, P0.05]，[ (32.55±4.44) (33.12±4.12) (27.22±6.48) U·g-1, P0.05]，MDA含量明显降低[(2.06土0.32) (2.05±0.30) (2.56±0.60) nmol mg-1, P0.05]。大脑切片HE染色表明牛磺酸可以改善大鼠海马组织的病理损伤。结论—：牛磺酸在400-600mg·kg-1d-1剂量范围内可显著地改善AD模型大鼠的学习记忆能力，，其机制可能与其抗氧化、改善胆碱能系统的功能及修复受损海马组织有关。
[Abstract]:Aim: to study the effect of taurine on learning and memory ability in Alzheimer's disease (AD) rats. Methods: male SD rats were randomly divided into normal group, sham operation group, model group, positive treatment group, taurine large, medium and small dose groups. The AD model was made by microinjection of 尾 -amyloid peptide1-40 (A 尾 1-40) into hippocampus. The positive group was treated by intragastric administration of Haberin. The middle and small dose groups were treated with different doses of taurine 600400mg kg-1 d-1 for 4 weeks. Morris water maze was used for behavioral test. After 24 h of water maze test, brain was taken from rat head, acetylcholine choline acetylcholine in hippocampus and cortex, acetylcholine Esterase and acetylcholinesterase in hippocampus and cortex were measured. Choline Acetyltransterase, superoxide dismutase (SOD), malondialdehyde (malondialdehyde), malondialdehyde (MDA), malondialdehyde (MDA). The activity of glutathione peroxidase (Glutathione peroxidase) GSH-Px) and the pathological changes in hippocampus of AD rats were observed by HE staining. Results in the water maze experiment, the escape latency in the taurine group was significantly shorter than that in the model group [39.08 卤5.23] [39.08 卤5.23], while in the taurine group, the number of platform penetration and the third quadrant swimming time were significantly longer than those in the model group [4.38 卤1.06L, 4.10 卤1.10 卤2.89 卤1.69)P0.05], [38.90 卤3.35: 3892 卤3.31 卤34.96 卤4.30sP0.05]. Compared with the model group, the content of Ach and the activity of ChAT in hippocampal tissue of the high dose group were significantly increased [159.06 卤13.160.10 卤9.88U 144.50 卤17.39U / ml p0.05], [225.36 卤22.30U 222.12 卤21.41201 卤21.41201.67 卤33.80U / g] significantly decreased [122.25 卤11.99120.45 卤11.20143.11 卤19.68Umgprot0.05]. In the taurine group, the content of Ach and the activity of ChAT in the cortex of the high-dose group were significantly increased [160.31 卤12.64hu 159.10 卤9.83U], [214.81 卤20.176.06 卤27.136.06 卤27.130.06 卤27.134IUP / g0.05], and the activity of Ache was significantly decreased [118.88 卤12.43U 117.05 卤8.96U / mg proprot1]; in taurine, the activity of Ache was significantly decreased [118.88 卤12.43U / mg / g / g]; in the taurine group, the activity of Ache was significantly lower than that in the control group (P < 0.05). In the high-dose group, the activity of GSH-PX in hippocampus increased significantly [209.38 卤34.48) (209.33 卤29.67) and 179.78 卤28.38) U mg-1, P0.05], [35.71 卤7.66 卤35.36 卤6.63], 28.77 卤8.12, P0.05], and the content of MDA decreased significantly [1.93 卤0.32, 1.89, 0.30, 2.38 卤0.52 nmol mg-1, P0.05]. In the taurine group, the activity of GSH-PX in the cortex of the high-dose group was significantly increased [199.38 卤31.22) (201.05 26.93) (172.00 卤16.46 U mg-1, P0.05), [32.55 卤4.44) (33.12 卤4.12) 渭 g-1, P0.05] decreased significantly [2.06 卤0.32) (2.05 卤0.30) (2.56 卤0.60) nmol mg-1g, P0.05]. He staining of brain slices showed that taurine could improve the pathological injury of hippocampus in rats. Conclusion: taurine can significantly improve the learning and memory ability of AD model rats within the range of 400-600mg kg-1d-1 dosage, and its mechanism may be related to its antioxidation, improving the function of cholinergic system and repairing damaged hippocampal tissue.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R749.16;R-332

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