College of Pharmacy and Medical Research Center, Chungbuk National University, 194-31 Osongsaemgmyeong 1-ro, Osong-eup, Heungdeok-gu, Cheongju 28160, Chungbuk, Korea.
Int J Mol Sci. 2017 Nov 28;18(12):2554. doi: 10.3390/ijms18122554.
Oxidative stress and neuroinflammation are implicated in the development and pathogenesis of Alzheimer's disease (AD). Here, we investigated the anti-inflammatory and antioxidative effects of krill oil. Oil from (Antarctic krill), an Antarctic marine species, is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). We examined whether krill oil diet (80 mg/kg/day for one month) prevents amyloidogenesis and cognitive impairment induced by intraperitoneal lipopolysaccharide (LPS) (250 µg/kg, seven times daily) injections in AD mice model and found that krill oil treatment inhibited the LPS-induced memory loss. We also found that krill oil treatment inhibited the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and decreased reactive oxygen species (ROS) and malondialdehyde levels. Krill oil also suppresses IκB degradation as well as p50 and p65 translocation into the nuclei of LPS-injected mice brain cells. In association with the inhibitory effect on neuroinflammation and oxidative stress, krill oil suppressed amyloid beta (1-42) peptide generation by the down-regulating APP and BACE1 expression in vivo. We found that eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (50 and 100 µM) dose-dependently decreased LPS-induced nitric oxide and ROS generation, and COX-2 and iNOS expression as well as nuclear factor-κB activity in cultured microglial BV-2 cells. These results suggest that krill oil ameliorated impairment via anti-inflammatory, antioxidative, and anti-amyloidogenic mechanisms.
氧化应激和神经炎症与阿尔茨海默病(AD)的发展和发病机制有关。在这里,我们研究了磷虾油的抗炎和抗氧化作用。南极磷虾(Antarctic krill)是一种南极海洋物种,其油富含二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)。我们研究了磷虾油饮食(每天 80 毫克/千克,持续一个月)是否可以预防内毒素脂多糖(LPS)(250µg/kg,每天 7 次)腹腔注射诱导的 AD 小鼠模型中的淀粉样蛋白形成和认知障碍,结果发现磷虾油治疗可抑制 LPS 诱导的记忆丧失。我们还发现磷虾油治疗可抑制 LPS 诱导的诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达,并降低活性氧(ROS)和丙二醛水平。磷虾油还抑制 IκB 降解以及 p50 和 p65 向 LPS 注射小鼠脑细胞核内易位。与抑制神经炎症和氧化应激有关,磷虾油通过下调 APP 和 BACE1 的表达来抑制体内淀粉样β肽(1-42)的产生。我们发现,二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)(50 和 100µM)可剂量依赖性地降低 LPS 诱导的一氧化氮和 ROS 生成,以及 COX-2 和 iNOS 表达以及核因子-κB 活性在体外培养的小胶质细胞 BV-2 细胞中。这些结果表明,磷虾油通过抗炎、抗氧化和抗淀粉样形成机制改善了损伤。