食用特級初榨橄欖油(extra virgin olive oil)如何精確地有助于降低患上阿爾茨海默病(Alzheimer's disease,, AD)的風險是一個謎。在一項新的研究中,研究人員報道解決這個謎的關鍵可能在于橄欖油中的一種組分,,這個組分有助于將異常的AD蛋白從大腦中運輸出去,。相關研究結果于2013年2月15日在線發(fā)表在ACS Chemical Neuroscience期刊上,論文標題為“Olive-Oil-Derived Oleocanthal Enhances β-Amyloid Clearance as a Potential Neuroprotective Mechanism against Alzheimer’s Disease: In Vitro and in Vivo Studies”,。
Amal Kaddoumi和同事們注意到在全世界,,AD影響著大約數(shù)千萬人,但是它的發(fā)病率在地中海國家中比較低,??茖W家們曾經(jīng)將它歸結于橄欖油中高含量的有益于健康的單不飽和脂肪,因而這些單不飽和脂肪在地中海飲食中被大量食用,。新近的研究提示著這種實際的保護性試劑可能是一種被稱作刺激醛(Oleocanthal)的物質,。這種物質阻止神經(jīng)細胞在AD中遭受損傷。
在最新的這項研究中,,Kaddoumi和同事們尋求證據(jù)來證實橄欖油刺激醛是否有助于降低大腦中的β-淀粉樣蛋白(beta-amyloid,, Aβ)堆積,其中這種堆積被認為是AD的罪魁禍首,。
作為對人研究的替代,,他們追蹤了橄欖油刺激醛在實驗室小鼠大腦和體外培養(yǎng)的小鼠大腦細胞中的影響。在這種實驗中,,橄欖油刺激醛持續(xù)地促進兩種蛋白和關鍵性酶的產生,,其中這些蛋白和酶被認為在移除大腦內Aβ中發(fā)揮著關鍵性作用。論文結論為“在地中海飲食中,,源自特級初榨橄欖油的刺激醛潛在地降低患上AD或相關的神經(jīng)元退行性癡呆癥的風險。”(生物谷Bioon.com)
DOI: 10.1021/cn400024q
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Olive-Oil-Derived Oleocanthal Enhances β-Amyloid Clearance as a Potential Neuroprotective Mechanism against Alzheimer’s Disease: In Vitro and in Vivo Studies
Alaa H-Abuznait , Hisham Qosa , Belnaser A-Busnena , Khalid A-El Sayed and Amal Kaddoumi.
Oleocanthal, a phenolic component of extra-virgin olive oil, has been recently linked to reduced risk of Alzheimer’s disease (AD), a neurodegenerative disease that is characterized by accumulation of β-amyloid (Aβ) and tau proteins in the brain. However, the mechanism by which oleocanthal exerts its neuroprotective effect is still incompletely understood. Here, we provide in vitro and in vivo evidence for the potential of oleocanthal to enhance Aβ clearance from the brain via up-regulation of P-glycoprotein (P-gp) and LDL lipoprotein receptor related protein-1 (LRP1), major Aβ transport proteins, at the blood-brain barrier (BBB). Results from in vitro and in vivo studies demonstrated similar and consistent pattern of oleocanthal in controlling Aβ levels. In cultured mice brain endothelial cells, oleocanthal treatment increased P-gp and LRP1 expression and activity. Brain efflux index (BEI%) studies of 125I-Aβ40 showed that administration of oleocanthal extracted from extra-virgin olive oil to C57BL/6 wild-type mice enhanced 125I-Aβ40 clearance from the brain and increased the BEI% from 62.0 ± 3.0% for control mice to 79.9 ± 1.6% for oleocanthal treated mice. Increased P-gp and LRP1 expression in the brain microvessels and inhibition studies confirmed the role of up-regulation of these proteins in enhancing 125I-Aβ40 clearance after oleocanthal treatment. Furthermore, our results demonstrated significant increase in 125I-Aβ40 degradation as a result of the up-regulation of Aβ degrading enzymes following oleocanthal treatment. In conclusion, these findings provide experimental support that potential reduced risk of AD associated with extra-virgin olive oil could be mediated by enhancement of Aβ clearance from the brain.