Yuan Hai-feng, Li Xi, Quan Qian-kun, Wang Ning-ning, Li Yuan, Li Ming
Department of Neurology, the Second Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an 710004, Shaanxi Province, China.
Zhong Xi Yi Jie He Xue Bao. 2010 Feb;8(2):152-7. doi: 10.3736/jcim20100210.
To investigate the effects of Naoerkang (NEK), a compound traditional Chinese herbal medicine, on the expressions of beta-amyloid peptide 1-42 (Abeta(1-42)) and neprilysin (NEP) in hippocampal tissues in a rat model of Alzheimer's disease (AD).
Forty-eight male SD rats were randomly divided into normal control group, untreated group, piracetam group, low-dose NEK group, medium-dose NEK group, and high-dose NEK group, with 8 rats in each group. Five microliters of Abeta(1-42) (2 microg/microL) were injected into CA1 area of hippocampus in rat to establish AD model whereas the normal control rats were injected with same volume of normal saline for comparison. The rats in the NEK groups were treated respectively with high-, medium- and low-dose [60, 30, 15 g/(kg.d)] NEK for 28 days consecutively; piracetam [0.375 g/(kg.d)] was intragastrically administered to rats in the piracetam group; and normal saline was applied in the control and untreated groups. Y-maze test was used for behavioral study to test the learning and memory abilities of rats in different groups. The expressions of Abeta(1-42) and NEP in hippocampus were determined by immunohistochemical method, and the results were analyzed by image acquisition and analysis system.
Injection of Abeta(1-42) could induce learning and memory dysfunction and up-regulate Abeta(1-42) expression in hippocampal tissue in rats of the untreated group. Compared with the normal control group, the abilities of learning and memory of rats in the untreated group were significantly decreased (P<0.01) and the expression of Abeta(1-42) was significantly increased (P<0.01) after model establishment. After 28-day administration of NEK and piracetam, the abilities of learning and memory of AD rats in piracetam and low-dose, medium-dose and high-dose NEK groups were significantly improved as compared with the untreated group (P<0.01 or P<0.05); the expression of Abeta(1-42) in hippocampal tissues was decreased (P<0.01 or P<0.05) and the expression of NEP was increased (P<0.01 or P<0.05), especially in the high-dose NEK group.
NEK can play the role of anti-dementia by increasing the expression of NEP in hippocampal tissues of AD rats so as to reduce the quantity of AAbeta(1-42) and by improving the ability of learning and memory of rats with AD.
研究中药复方脑尔康（NEK）对阿尔茨海默病（AD）大鼠模型海马组织中β-淀粉样肽1-42（Abeta(1-42)）和中性内肽酶（NEP）表达的影响。
将48只雄性SD大鼠随机分为正常对照组、未治疗组、吡拉西坦组、低剂量NEK组、中剂量NEK组和高剂量NEK组，每组8只。将5微升Abeta(1-42)（2微克/微升）注射到大鼠海马CA1区以建立AD模型，而正常对照大鼠注射相同体积的生理盐水作对照。NEK组大鼠分别连续28天给予高、中、低剂量[60、30、15克/（千克·天）]NEK；吡拉西坦组大鼠灌胃给予吡拉西坦[0.375克/（千克·天）]；对照组和未治疗组给予生理盐水。采用Y迷宫试验进行行为学研究，以测试不同组大鼠的学习和记忆能力。用免疫组织化学方法检测海马中Abeta(1-42)和NEP的表达，结果通过图像采集与分析系统进行分析。
注射Abeta(1-42)可诱导未治疗组大鼠学习和记忆功能障碍，并上调海马组织中Abeta(1-42)的表达。与正常对照组相比，未治疗组大鼠模型建立后学习和记忆能力显著下降（P<0.01），Abeta(1-42)表达显著增加（P<0.01）。给予NEK和吡拉西坦28天后，与未治疗组相比，吡拉西坦组以及低、中、高剂量NEK组AD大鼠的学习和记忆能力显著改善（P<0.01或P<0.05）；海马组织中Abeta(1-42)表达降低（P<0.01或P<0.05），NEP表达增加（P<0.01或P<0.05），尤其是高剂量NEK组。
NEK可通过增加AD大鼠海马组织中NEP的表达以减少Abeta(1-42)的量，并改善AD大鼠的学习和记忆能力，从而发挥抗痴呆作用。
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