本文選題：�；撬� + β淀粉樣肽　； 參考：《青島大學(xué)》2012年碩士論文

【摘要】：目的：研究�；撬釋Π柎暮Ｄ�(Alzheimer's disease,AD)大鼠學(xué)習記憶能力的影響。 方法：雄性SD大鼠,隨機分為正常組、假手術(shù)組、模型組、陽性治療組、牛磺酸大、中、小劑量組。海馬微量注射凝聚態(tài)β淀粉樣肽1-40(β-amyloid peptide1-40, Aβ1-40)制作AD模型,陽性治療組采用哈伯因灌胃治療,�；撬岽�、中、小劑量組采用不同劑量(600、400、200mg·kg-1·d-1)�；撬峁辔钢委�4周。用Morris水迷宮進行行為學(xué)測試,水迷宮測試完畢24h,大鼠斷頭取腦,測定海馬和皮質(zhì)中乙酰膽堿(Acetylcholine,Ach)、乙酰膽堿酯酶(Acetylcholine Esterase,Ache).乙酰膽堿轉(zhuǎn)移酶(Choline Acetyltransterase,ChAT)、超氧化物歧化酶(Superoxide Dismutase,SOD)、丙二醛(Malondialdehyde,MDA).谷胱甘肽過氧化物酶(Glutathione Peroxidase,GSH-Px)的活性,大腦切片HE染色觀察AD模型大鼠海馬病理學(xué)改變。 結(jié)果：Morris水迷宮實驗,�；撬嶂�、大劑量組逃避潛伏期均明顯比模型組縮短[(39.08±5.23)(39.11±2.24)(43.21±3.46)s,P0.05]；�；撬嶂�、大劑量組穿站臺次數(shù)和第三象限游泳時間均比模型組明顯延長[(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]。與模型組相比,�；撬嶂�、大劑量組海馬組織中Ach含量和ChAT活性均明顯增加[(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活性明顯降低[(122.25±11.99)(120.45±11.20)(143.11±19.68)U/mgprot,P0.05]。�；撬嶂�、大劑量組皮質(zhì)組織中Ach含量和ChAT活性均明顯增加[(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活性明顯降低[(118.88±12.43)(117.05±8.96)(139.37±11.81)U/mgprot,P0.05]；�；撬嶂小⒋髣┝拷M海馬組織中SOD、GSH-PX活性明顯增加[(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含量明顯降低[(1.93±0.32)(1.89 + 0.30) (2.38±0.52) nmol·mg-1, P0.05]。�；撬嶂�、大劑量組皮質(zhì)組織中SOD、GSH-PX活性明顯增加[(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含量明顯降低[(2.06土0.32) (2.05±0.30) (2.56±0.60) nmol mg-1, P0.05]。大腦切片HE染色表明�；撬峥梢愿纳拼笫蠛ｑR組織的病理損傷。 結(jié)論—：�；撬嵩�400-600mg·kg-1d-1劑量范圍內(nèi)可顯著地改善AD模型大鼠的學(xué)習記憶能力，，其機制可能與其抗氧化、改善膽堿能系統(tǒng)的功能及修復(fù)受損海馬組織有關(guān)。
[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 鹵5.23] [39.08 鹵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 鹵1.06L, 4.10 鹵1.10 鹵2.89 鹵1.69)P0.05], [38.90 鹵3.35: 3892 鹵3.31 鹵34.96 鹵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 鹵13.160.10 鹵9.88U 144.50 鹵17.39U / ml p0.05], [225.36 鹵22.30U 222.12 鹵21.41201 鹵21.41201.67 鹵33.80U / g] significantly decreased [122.25 鹵11.99120.45 鹵11.20143.11 鹵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 鹵12.64hu 159.10 鹵9.83U], [214.81 鹵20.176.06 鹵27.136.06 鹵27.130.06 鹵27.134IUP / g0.05], and the activity of Ache was significantly decreased [118.88 鹵12.43U 117.05 鹵8.96U / mg proprot1]; in taurine, the activity of Ache was significantly decreased [118.88 鹵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 鹵34.48) (209.33 鹵29.67) and 179.78 鹵28.38) U mg-1, P0.05], [35.71 鹵7.66 鹵35.36 鹵6.63], 28.77 鹵8.12, P0.05], and the content of MDA decreased significantly [1.93 鹵0.32, 1.89, 0.30, 2.38 鹵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 鹵31.22) (201.05 26.93) (172.00 鹵16.46 U mg-1, P0.05), [32.55 鹵4.44) (33.12 鹵4.12) 渭 g-1, P0.05] decreased significantly [2.06 鹵0.32) (2.05 鹵0.30) (2.56 鹵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.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2012
【分類號】：R749.16;R-332

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