中文摘要：

目的：考察白术多糖对D-半乳糖致衰老模型小鼠学习记忆的影响及其抗氧化作用。方法：采用小鼠颈背部皮下注射D．半乳糖溶液200mg·kg^-1·d-建立衰老模型；造模成功后，分成模型对照组，维生素E组，白术多糖100mg·kg^-1组，白术多糖200mg·kg^-1组，连续给药6周后检测小鼠行为学指标，以及血及脑组织中的丙二醛（MDA）、单胺氧化酶（MAO）、脂褐素（Lipo）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH．Px）、过氧化氢酶（CAT）、总抗氧化能力（T—AOC）等指标。结果：与模型对照组比较，白术多糖100mg·kg^-1能明显缩短衰老模型小鼠Morris水迷宫的逃逸潜伏期，缩短游泳路程，降低血清及脑组织中的MDA，Lipo含量及MAO的活性，升高血清中GSH．Px，CAT活性及T—AOC含量以及脑组织中的SOD，T-AOC活性；白术多糖200mg·kg^-1能显著降低小鼠血清及脑组织中的MDA，Lipo含量及MAO活性，升高小鼠血清中的SOD，GSH—Px，CAT活性以及脑组织中的SOD，T．AOC活性。结论：白术多糖能抑制机体内脂质过氧化物的生成，增强抗氧化酶的活性，从而提高衰老小鼠的抗氧化能力；可降低衰老小鼠脑组织中MAO的浓度，减少Lipo的生成、堆积，改善其学习记忆，推测可能有延缓衰老的作用。

英文摘要：

Objective： To investigate the effect of polysaccharides from Atractylodes macrocephala on learn- ing and memory and the antioxidantive property in D-galactose-induced aging mice. Methods： Each ICR mouse was daily received with cervix subcutaneous injections of 200 mg· kg^-1 D-galactose for 8 weeks to establish aging model. Successful model mice were treated with vitamin E and polysaccharides from Atractylodes macrocephal （ 100 and 200 mg· kg^-1 ） for 6 weeks. During this period, the behaviors and the levels of indicators in the blood and brain were detected. The indicators included malondialdehyde （MDA）, monoamine oxidase （MAO）, lipofuscin （ Lipo）, superoxide dismutase （ SOD）, glutathione peroxidase （ GSH-Px）, hydrogen peroxidase （ CAT）, and total anti-oxidatant capacity （T-AOC）. Results： Compared with aging control, polysaccharides from Atractylodes macro- cephal （100 mg·kg^-1） significantly shortened the escape-eclipse periods and distance of swim in the Morris water maze test, and reduced the levels of MDA, Lipo and the activity of MAO in serum and brain tissue. The polysac-charides increased serum GSH-Px, CAT and T-AOC activities, and brain SOD and T-AOC activities in aging mice. The polysaccharides at 200 mg·kg^-1 reduced MDA and Lipo levels, and MAO activity in serum and brain tissue; increased serum of SOD, GSH-Px and CAT activities, and brain SOD and T-AOC activities in aging mice. Conclu- sions： The polysaccharides of Atractylodes macrocephala can inhibit the generatio antioxidant enzyme activities, so that significantly increase the antioxidant ability also enhance the learning and memory functions. Therefore, they might delay the n of lipid peroxides and increase in the body. The polysaccharides aging process m mice