RT Journal Article
SR Electronic
T1 Allicin can reduce neuronal death and ameliorate the spatial memory impairment in Alzheimers disease models
JF Neurosciences Journal
JO Neurosciences (Riyadh)
FD Prince Sultan Military Medical City
SP 237
OP 243
VO 15
IS 4
A1 Li, Xian-Hui
A1 Li, Chun-Yan
A1 Xiang, Zhi-Gang
A1 Zhong, Fei
A1 Chen, Zheng-Ying
A1 Lu, Jiang-Ming
YR 2010
UL http://nsj.org.sa/content/15/4/237.abstract
AB OBJECTIVE: To investigate the mechanisms and protective effects of allicin on learning and memory in a mouse model of Alzheimer’s disease (AD).METHODS: 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 (AÕ[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 AÕ(1-42)+PBS group, and the AÕ(1-42)+allicin group. The AÕ(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 AÕ(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.RESULTS: The AÕ(1-42)-infused allicin-treated group showed significantly shorter latency times than the PBS treated AÕ(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 AÕ and p38MAPK expressions in the cerebral cortex of AD mice model (p=0.031).CONCLUSION: 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 AÕ and p38MAPK in the brain.