Hericium erinaceus polysaccharides (HEP) protect against gastric mucosa injury via modulating inflammatory factors, promoting antioxidant activity, and activating the PI3K-AKT pathway
文献类型: 外文期刊
作者: Weijun Cui;Xiangyang Zhu;Xueping Li;Xinling Song;Le Jia;Chen Zhang
作者机构:
关键词: Gastric mucosal injury;Hericium erinaceus;NO;PI3K/AKT;Polysaccharides
期刊名称: Food Innovation and Advances
ISSN: 2836-774X
年卷期: 2025 年 4 卷 3 期
页码:
收录情况: 无来源刊(2025版)
摘要: Gastric mucosal injury (GMI) is a common pathology affecting many people around the world. Hericium erinaceus polysaccharides (HEP) have various biological activities, such as anti-inflammatory, anti-oxidation, and protection of the gastrointestinal tract. HEP-1, a low molecular weight polysaccharide (1.67 × 104 Da) isolated from Hericium erinaceus, is composed of →6)-β-D-Glcp-(1→, →3)-β-D-Glcp-(1→, β-D-Glcp-(1→, and →3,6)-β-D-Glcp-(1→. However, whether HEP has preventive efficacy against GMI is unknown. This study investigated the intervention effect and potential mechanism of HEP-1 on GMI. Mice treated with HEP-1 for two weeks were treated with ethanol to induce gastric mucosal damage. The gastric mucosal tissue pathology, gastric tissue inflammatory factors, and gastric oxidative stress function were evaluated. The results showed that HEP-1 increased the activity of antioxidant enzymes, reduced the release of inflammatory factors, promoted the production of nitric oxide (NO), inhibited the production of endothelin-1 (ET-1), and increased the blood flow of gastric mucosa to maintain the defensive function of the gastric mucosa. HEP-1 also activated the PI3K-AKT signaling pathway, increased the expression of endothelial nitric oxide synthase (eNOS), promoted the expression of serum and glucocorticoid-induced kinase (SGK), and enhanced the biosynthesis of epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), thereby facilitating the repair and healing of gastric mucosal injury (GMI). Therefore, HEP-1 has the potential to preserve the integrity of the gastric mucosa and is anticipated to be a key bioactive ingredient in the prevention and repair of GMI.
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