Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food Science and Pharmaceutics, Zhejiang Ocean University, Zhoushan 316022, China.
Key Laboratory of Vector Biology and Pathogen Control of Zhejiang Province, Huzhou University, Huzhou Cent Hosp, Huzhou 313000, China.
Oxid Med Cell Longev. 2020 Aug 25;2020:1813798. doi: 10.1155/2020/1813798. eCollection 2020.
Hemp seed has been used as a traditional oriental medicine and health food in China for centuries. Polysaccharides from hemp seed (HSP) exhibit important properties of intestinal protection, but there are limited data on the specific underlying mechanism. The primary objective of this study was to investigate the protective effect of HSP on intestinal oxidative damage induced by cyclophosphamide (Cy) in mice. The results showed that pretreatment with HSP significantly increased the average daily gain, thymus index, spleen index, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activity in serum and ileal homogenate and significantly reduced malondialdehyde (MDA) content in ileal homogenate. In addition, the expression levels of SOD, GSH-Px, Nrf2, heme oxidase-1 (HO-1), and quinoneoxidoreductase-1 (NQO1) mRNA in ileal homogenate were significantly increased. Western blot results showed that HSP significantly upregulated the expression of Nrf2 protein and downregulated the expression of Keap1 protein in the ileum. Collectively, our findings indicated that HSP had protective effects on intestinal oxidative damage induced by Cy in mice, and its mechanism might be related to the activation of Nrf2-Keap1 signaling pathway.
麻籽作为一种传统的东方医学和保健食品，在中国已经有几个世纪的历史了。麻籽多糖（HSP）具有重要的肠道保护特性，但关于其具体的潜在机制的数据有限。本研究的主要目的是研究 HSP 对环磷酰胺（Cy）诱导的小鼠肠道氧化损伤的保护作用。结果表明，HSP 预处理可显著增加平均日增重、胸腺指数、脾脏指数、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）在血清和回肠匀浆中的活性，并显著降低回肠匀浆中的丙二醛（MDA）含量。此外，回肠匀浆中 SOD、GSH-Px、Nrf2、血红素加氧酶-1（HO-1）和醌氧化还原酶-1（NQO1）mRNA 的表达水平也显著升高。Western blot 结果表明，HSP 可显著上调 Nrf2 蛋白的表达，下调 Keap1 蛋白在回肠中的表达。综上所述，本研究结果表明 HSP 对 Cy 诱导的小鼠肠道氧化损伤具有保护作用，其机制可能与 Nrf2-Keap1 信号通路的激活有关。
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