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五味子乙素保护PC12细胞免受神经退行性疾病氧化应激的影响。

Schisandrin B protects PC12 cells against oxidative stress of neurodegenerative diseases.

作者信息

Jiang En-Ping, Li He, Yu Chun-Rong, Yu Chun-Yan, Jing Shu, Sun Hong-Xia, Wang Chun-Mei, Fan Xin-Tian, Chen Jian-Guang, Wang Sen

机构信息

aCancer Institute, Guangdong Medical College, Dongguan bCollege of Pharmacy cCollege of Basic Medical, Beihua University dBeihua University Affiliated Hospital, Jilin eJOINN Laboratories, Beijing, China.

出版信息

Neuroreport. 2015 Apr 15;26(6):360-6. doi: 10.1097/WNR.0000000000000354.

DOI:10.1097/WNR.0000000000000354
PMID:25756908
Abstract

Increasing evidence places Schisandrin B (Sch B) at an important position in nerve protection, indicating that Sch B might play a positive role in the therapy of neurodegenerative diseases. However, there is little information on it. Our studies showed that pretreatment with Sch B could reduce lactate dehydrogenase, malondialdehyde, and reactive oxygen species release and significantly increase the cell viability and the superoxide dismutase level. Sch B (10 μM) markedly inhibited cell apoptosis, whereas LY294002 (20 μM), a phosphatidylinositol-3 kinase inhibitor, blocked the antiapoptotic effect. More importantly, Sch B (10 μM) increased the phosphoprotein kinase B/protein kinase B (Akt) and B-cell lymphoma-2/Bcl-2 associated X protein ratios on preincubation with cells for 2 h, which was then inhibited by LY294002 (20 μM). Results indicate that Sch B can protect PC12 cells from apoptosis by activating the phosphatidylinositol-3 kinase/Akt signaling pathway and may emerge as a potential drug for neurodegenerative diseases.

摘要

越来越多的证据表明五味子乙素(Sch B)在神经保护中占据重要地位,这表明Sch B可能在神经退行性疾病的治疗中发挥积极作用。然而,关于它的信息却很少。我们的研究表明,Sch B预处理可降低乳酸脱氢酶、丙二醛和活性氧的释放,并显著提高细胞活力和超氧化物歧化酶水平。Sch B(10 μM)显著抑制细胞凋亡,而磷脂酰肌醇-3激酶抑制剂LY294002(20 μM)可阻断其抗凋亡作用。更重要的是,Sch B(10 μM)在与细胞预孵育2小时后可提高磷酸化蛋白激酶B/蛋白激酶B(Akt)和B细胞淋巴瘤-2/Bcl-2相关X蛋白的比例,随后被LY294002(20 μM)抑制。结果表明,Sch B可通过激活磷脂酰肌醇-3激酶/Akt信号通路保护PC12细胞免受凋亡,可能成为治疗神经退行性疾病的潜在药物。

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