Abstract

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.

Highlights

  • Oxidative stress is defined as the imbalance between oxygen free radicals and antioxidants [1]

  • The previous study has shown that oxidative stress was a major factor causing several tissue injuries in intestinal ischemia and reperfusion (I/R) [5]

  • The results showed that HSP significantly increased the levels of superoxide dismutase (SOD) and GSH-Px mRNA in ileal tissues, which was consistent with the results of measurements of antioxidant enzymes SOD and GSH-Px levels

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Summary

Introduction

Oxidative stress is defined as the imbalance between oxygen free radicals and antioxidants [1]. The intestinal tissue as important barrier is easy to be attacked by stressful conditions such as oxidative stress, resulting in an increase in permeation of toxins. When there is excessive accumulation of oxygen free radical, they may damage the intestinal mucosal barrier, increase intestinal mucosal permeability, and disorder intestinal flora in the intestine, thereby affecting the body’s steady state system [3, 4]. The previous study has shown that oxidative stress was a major factor causing several tissue injuries in intestinal ischemia and reperfusion (I/R) [5]. Oxidative stress is believed to be an important factor in the pathogenesis of intestinal inflammation [7,8,9].

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