首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Fumanjian, a Classic Chinese Herbal Formula, Can Ameliorate the Impairment of Spatial Learning and Memory through Apoptotic Signaling Pathway in the Hippocampus of Rats with Abeta_(1-40) -Induced Alzheimer's Disease
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Fumanjian, a Classic Chinese Herbal Formula, Can Ameliorate the Impairment of Spatial Learning and Memory through Apoptotic Signaling Pathway in the Hippocampus of Rats with Abeta_(1-40) -Induced Alzheimer's Disease

机译:佛南亚,经典的中草原公式,可以通过大鼠海马海马(1-40)诱导阿尔茨海默病的凋亡信号通路来改善空间学习和记忆的损害

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摘要

Alzheimer's disease (AD) is the most common form of dementia and lacks disease-altering treatments. Fumanjian (FMJ), a famous classic Chinese herbal prescription for dementia, was first recorded in the Complete Works of Jingyue during the Ming Dynasty. This study aimed to investigate whether FMJ could prevent cognitive deficit and take neuroprotective effects in Abeta_(1-40)-induced rat model through apoptotic signaling pathway. AD model was established by bilateral injection of Abeta_(1-40) into hippocampus in rat. All rats were tested for their capabilities of spatial navigation and memorization by Morris water maze. Apoptosis was tested using TUNEL staining in hippocampus neuronal cells; RT-PCR tested expression of Bcl-2 and Bax mRNA; western blotting tested protein level of cleaved caspase-3. After 14 days of treatment, FMJ significantly improved the escape latency and enhanced platform-cross number compared with the Abeta_(1-40)-injected group (P < 0.05 or P < 0.01). FMJ also significantly decreased number of TUNEL-positive neuronal apoptosis and the expressions of Bax and cleaved Caspase-3 and increased the expression of Bcl-2 (P < 0.01) compared with AD model group. In conclusion, FMJ exerts a protective effect against Abeta_(1-40)-induced learning and memory deficits and neuronal apoptosis, suggesting that FMJ could be used as a potential therapeutic formula for AD.
机译:阿尔茨海默病(AD)是最常见的痴呆形式,缺乏疾病改变治疗。 Fumanjian(FMJ)是一个着名的痴呆症的中草药处方,首先在明代的完整作品中记录。本研究旨在调查FMJ是否可以通过凋亡信号通路在Abeta_(1-40)诱导的大鼠模型中对认知缺陷和对神经保护作用进行神经保护作用。通过双侧注射到大鼠海马的Abeta_(1-40)建立广告模型。所有大鼠都测试了它们的空间导航能力和Morris水迷宫的记忆。使用海马神经元细胞中的TUNEL染色测试细胞凋亡; RT-PCR测试Bcl-2和Bax mRNA的表达;蛋白质印迹测试蛋白水平的切割的Caspase-3。处理14天后,与ABETA_(1-40) - 注射组(P <0.05或P <0.01)相比,FMJ显着改善了逃逸潜伏期和增强的平台交叉数。 FMJ还显着降低了Tueel阳性神经元细胞凋亡的数量和Bax和Cleaved Caspase-3的表达,并与AD模型组相比,增加了Bcl-2(P <0.01)的表达。总之,FMJ对ABETA_(1-40)引起的学习和记忆缺陷和神经元凋亡产生了保护作用,表明FMJ可以用作广告的潜在治疗公式。

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