發(fā)布日期：2016-04-18

帕金森病（Parkinson's disease）又稱"震顫麻痹"，巴金森氏癥或柏金遜癥，是老年人中第四位最常見的神經(jīng)變性疾病,全球大約400萬患者，將近50%在中國,未來5-10年中國的患者將達到500萬人，在中國已經(jīng)稱為老年人的第3大殺手。本病在≥65歲的人群中患病機率為1.7%，在＞40歲中為0.4%，也可在兒童期或青春期發(fā)病，發(fā)病年齡呈越來越低的趨勢。帕金森病的病變部位在人腦的中腦部位，該處有一群神經(jīng)細胞叫黑質(zhì)神經(jīng)元，它們通過合成一種“多巴胺”的神經(jīng)遞質(zhì)，對大腦的運動功能進行調(diào)控。當這些黑質(zhì)神經(jīng)元變性死亡達８０％以上時，就會出現(xiàn)帕金森病的癥狀。雖然該病的發(fā)病機理目前還不透徹，但是越來越多的證據(jù)表明，該病的發(fā)生與氧化應(yīng)激密切相關(guān)。該病最主要的危害就是失去自主控制運動的能力。

08年7月，日本名古屋大學的科學家用【DHA hydroperoxide (DHA-OOH) 和 6-hydroxydopamine (6-OHDA)（能誘導細胞產(chǎn)生活性氧的物質(zhì)）】處理能產(chǎn)生多巴胺的神經(jīng)元細胞，結(jié)果在細胞間檢測到活性氧的存在，絕大多數(shù)細胞線粒體功能紊亂，細胞進行性 性死亡，而當研究人員用蝦青素預處理細胞后，蝦青素能顯著地減少細胞活性氧的產(chǎn)生，顯著減少線粒體紊亂的發(fā)生，能大大提高細胞的存活率。當檢測蝦青素在細 胞中的分布，發(fā)現(xiàn)蝦青素在線粒體中的濃度最高，而線粒體的呼吸鏈是活性氧產(chǎn)生的主要場所，因此，這也間接揭示了蝦青素保護線粒體功能正常，抗氧化提高細胞 存活的作用機理。由于蝦青素是目前自然界中抗氧化性最強，安全性高，還能透過血腦屏障的物質(zhì)，所以作者最后認為蝦青素有望成為預防和延緩帕金森病進程的首 選保健食品。

本研究的題為《Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism》，發(fā)表在2008年12月的《Brain Research》上

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Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism

Xuebo Liu, Takahiro Shibata, Shinsuke Hisaka, Toshihiko Osawa?
Laboratory of Food and Biodynamics, Graduate School of Bioagricultural Science, Nagoya University, Furo-cho, Nagoya 464-8601, Japan

Abstract:Astaxanthin is a powerful antioxidant that occurs naturally in a wide variety of living organisms. The aim of this study is to investigate the effect and the mechanism of astaxanthin on reactive oxygen species (ROS)-mediated apoptosis in dopaminergic SH-SY5Y cells. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA),either of which is ROS-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by MTT assay, whereas a significant protection was shown while the cells were pretreated with astaxanthin. Moreover, 100 nM astaxanthin pretreatment significantly inhibited apoptosis, mitochondrial abnormalities and 
intracellular ROS generation occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of astaxanthin is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is suggested that astaxanthin may be an effective treatment for oxidative stress-associated neurodegeneration.