Department of Geriatric Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Department of Epidemiology and Health Statistics, The School of Public Health of Qingdao University, Qingdao, Shandong, China.
Curr Eye Res. 2021 Jun;46(6):802-810. doi: 10.1080/02713683.2020.1842456. Epub 2020 Nov 6.
Alginate oligosaccharides (AOS), obtained from depolymerizing alginate, has multiple pharmacological benefits. Cataract is a common disease caused by turbidity of the lens protein due to lens metabolism disorders. This study aimed to test the effects and the underlying mechanisms of AOS on D-galactose (D-gal)-mediated cataract.
A total of 45 8-week-old C57BL/6 J male mice were randomly divided into 5 groups. After eight weeks' intervention, the score of cataract was calculated depending on the turbidity of the lens. Hematoxylin and eosin (HE) and transmission electron microscope (TEM) images detection kits, respectively. SOD1, SOD2, catalase (CAT) and p53 protein expressions were examined by Western blot. Nuclear factor erythroid-2 related factor (Nrf2) and heme oxygenase-1 (HO-1) mRNA expressions were examined by Quantitative Real Time-PCR (RT-qPCR).
The score of the turbidity of the lens showed that AOS significantly delayed the cataractogenesis. HE staining and TEM imaging showed that AOS decreased the damage and senescence of lenses in D-gal-induced C57BL/6 J mice. We further detected aging marker p53 expression in crystalline lenses, and our result showed that AOS significantly inhibited p53 protein expression in D-gal-induced mice. In addition, SOD activity and MDA level detection results showed that AOS significantly increased the activity of SOD, and decreased the level of MDA in crystalline lenses homogenates of D-gal-induced aging mice. Western blot results showed that AOS attenuated the damage of D-gal in the protein expressions of antioxidative enzymes SOD1, SOD2 and CAT. RT-qPCR results showed that AOS suppressed the down-regulation of Nrf2 and HO-1 mRNA expressions induced by D-gal.
AOS prevents against D-gal-mediated cataract in C57BL/6 J mice via inhibiting oxidative stress and up-regulating antioxidant system. Consequently, our results suggest that AOS may be an effective therapeutic strategy against cataract.
从海藻酸钠中解聚得到的海藻酸钠寡糖(AOS)具有多种药理作用。白内障是一种常见疾病,由于晶状体代谢紊乱导致晶状体蛋白混浊。本研究旨在测试 AOS 对 D-半乳糖(D-gal)诱导白内障的作用及其机制。
将 45 只 8 周龄 C57BL/6J 雄性小鼠随机分为 5 组。干预 8 周后,根据晶状体混浊程度计算白内障评分。分别采用苏木精和伊红(HE)染色和透射电镜(TEM)图像检测试剂盒,Western blot 检测 SOD1、SOD2、过氧化氢酶(CAT)和 p53 蛋白表达,定量实时 PCR(RT-qPCR)检测核因子红细胞 2 相关因子(Nrf2)和血红素加氧酶 1(HO-1)mRNA 表达。
晶状体混浊评分显示,AOS 可显著延缓白内障的发生。HE 染色和 TEM 成像显示,AOS 减轻了 D-gal 诱导的 C57BL/6J 小鼠晶状体的损伤和衰老。我们进一步检测了晶状体中衰老标志物 p53 的表达,结果显示 AOS 显著抑制了 D-gal 诱导的小鼠中 p53 蛋白的表达。此外,SOD 活性和 MDA 水平检测结果显示,AOS 显著提高了 D-gal 诱导衰老小鼠晶状体匀浆中 SOD 的活性,降低了 MDA 的水平。Western blot 结果显示,AOS 减轻了 D-gal 对抗氧化酶 SOD1、SOD2 和 CAT 蛋白表达的损伤。RT-qPCR 结果显示,AOS 抑制了 D-gal 诱导的 Nrf2 和 HO-1 mRNA 表达的下调。
AOS 通过抑制氧化应激和上调抗氧化系统,预防 C57BL/6J 小鼠的 D-gal 诱导白内障。因此,我们的结果表明,AOS 可能是一种有效的白内障治疗策略。