Li Xian-Hui, Li Chun-Yan, Xiang Zhi-Gang, Zhong Fei, Chen Zheng-Ying, Lu Jiang-Ming
Institute of Medicine of Jishou University, Jishou 416000, Hunan Province, China.
Neurosciences (Riyadh). 2010 Oct;15(4):237-43.
To investigate the mechanisms and protective effects of allicin on learning and memory in a mouse model of Alzheimer's disease (AD).
This study took place in the Institute of Medicine of Jishou University, Jishou, China, between January and September 2009. Allicin was given as preventive administration after AD was induced by amyloid beta (Aß[1-42]), and the protective effects of Allicin against learning and memory impairment were investigated. Sixty mice were randomly divided into 3 groups including the sham-operated+phosphate buffer solution (PBS) group, the Aß(1-42)+PBS group, and the Aß(1-42)+allicin group. The Aß(1-42) (1 µL = 4µg) was injected into the bilateral hippocampi. Sham-operated mice were infused with PBS. Allicin or PBS was then injected intraperitoneally for 14 days. The animals were trained, and learning and memory abilities tested using the Morris Water-Maze. The changes of Aß(1-42) and P38 mitogen-activated protein kinase (p38MAPK) were recorded to explore the mechanism of allicin's protective effects on learning and memory deficits.
The Aß(1-42)-infused allicin-treated group showed significantly shorter latency times than the PBS treated Aß(1-42)-infused group from the second day of learning sessions (p=0.031), accompanied with significant reduction of malondialdehyde (MDA) (p=0.035) and an increase of superoxide dismutase (SOD) activity (p=0.041). Allicin also decreased Aß and p38MAPK expressions in the cerebral cortex of AD mice model (p=0.031).
Preventive administration of allicin prevented learning and memory impairment, the mechanism may be due to an increase in the activity of SOD, a reduction in the levels of MDA and the expressions of Aß and p38MAPK in the brain.
探讨大蒜素对阿尔茨海默病(AD)小鼠模型学习和记忆的作用机制及保护作用。
本研究于2009年1月至9月在中国吉首大学医学院进行。在用β淀粉样蛋白(Aβ[1-42])诱导AD后给予大蒜素预防性给药,研究大蒜素对学习和记忆障碍的保护作用。60只小鼠随机分为3组,包括假手术+磷酸盐缓冲液(PBS)组、Aβ(1-42)+PBS组和Aβ(1-42)+大蒜素组。将Aβ(1-42)(1μL = 4μg)注入双侧海马。假手术小鼠注入PBS。然后腹腔注射大蒜素或PBS,持续14天。对动物进行训练,并使用Morris水迷宫测试学习和记忆能力。记录Aβ(1-42)和P38丝裂原活化蛋白激酶(p38MAPK)的变化,以探讨大蒜素对学习和记忆缺陷保护作用的机制。
从学习阶段的第二天起,Aβ(1-42)注入大蒜素治疗组的潜伏期明显短于PBS治疗的Aβ(1-42)注入组(p = 0.031),同时丙二醛(MDA)显著降低(p = 0.035),超氧化物歧化酶(SOD)活性增加(p = 0.041)。大蒜素还降低了AD小鼠模型大脑皮质中Aβ和p38MAPK的表达(p = 0.031)。
大蒜素预防性给药可预防学习和记忆障碍,其机制可能是由于大脑中SOD活性增加、MDA水平降低以及Aβ和p38MAPK表达减少。