食品科学 ›› 2022, Vol. 43 ›› Issue (9): 150-157.doi: 10.7506/spkx1002-6630-20210127-296

• 营养卫生 • 上一篇    下一篇

燕麦多糖对小鼠急性胃黏膜损伤的保护作用

丁丽婷,潘世杰,胡婕伦,钟亚东,赵明姣,吴婷,方芳,黄钻元,聂少平,尧梅香,钟虹光,谢明勇   

  1. (1.南昌大学 食品科学与技术国家重点实验室,中加食品科学技术联合实验室(南昌),江西 南昌 330047;2.江中食疗科技有限公司,江西 九江 330000)
  • 出版日期:2022-05-15 发布日期:2022-05-27
  • 基金资助:
    江西省“揭榜挂帅”关键技术类(首批)项目(20212AAF01005); 国家自然科学基金地区科学基金项目(31960464); 中国食品科学技术学会食品科技基金——江中食疗胃肠健康专项科研基金(2019-05); 江西省科技厅国家奖后备培育项目(20192AEI91004);江西省高端人才培育项目(20204BCJ24006); 食品科学与技术重点实验室目标导向项目(SKLF-ZZA-201911); 江西省生物活性多糖重点实验室项目(20212BCD42016);江西省重大科技创新平台培育项目(20194AFD44002); 江西省中央引导地方科技发展资金项目(20212ZDD02008)

Protective Effect of Oat Polysaccharides against Acute Gastric Mucosal Injury in Mice

DING Liting, PAN Shijie, HU Jielun, ZHONG Yadong, ZHAO Mingjiao, WU Ting, FANG Fang, HUANG Zuanyuan, NIE Shaoping, YAO Meixiang, ZHONG Hongguang, XIE Mingyong   

  1. (1. State Key Laboratory of Food Science and Technology, China-Canada Joint Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China; 2. Jiang Zhong Food Therapy Technology Co., Ltd., Jiujiang 330000, China)
  • Online:2022-05-15 Published:2022-05-27

摘要: 目的:探讨燕麦多糖对体积分数70%乙醇溶液致小鼠急性胃黏膜损伤的保护作用。方法:60 只雄性昆明小鼠随机均等分为正常组,模型组,阳性组(西米替丁100 mg/kg mb),燕麦多糖低、中、高剂量组(100、200、400 mg/kg mb),分别灌胃相应受试物;14 d后采用体积分数70%乙醇溶液建立急性胃黏膜损伤模型,测定脏器指数并进行胃黏膜损伤评价,同时测定胃液pH值、血清NO浓度及胃组织中白细胞介素10(interlrukin-10,IL-10)、脂多糖(lipopolysaccharide,LPS)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)、谷胱甘肽(glutathione,GSH)水平及胃蛋白酶活力。结果:与模型组相比,燕麦多糖各剂量组小鼠胃黏膜损伤明显减轻,燕麦多糖高剂量组效果最好,胃黏膜损伤抑制率达76.04%,各剂量燕麦多糖均能提高胃液pH值,血清NO浓度以及胃组织GSH、VEGF质量浓度和SOD活力,降低胃组织胃蛋白酶活力和LPS质量浓度,其中高剂量燕麦多糖对以上指标的改善效果显著。结论:燕麦多糖对乙醇致小鼠急性胃黏膜损伤具有明显的保护作用,其中燕麦多糖高剂量组保护效果最佳,作用机制可能和燕麦多糖能够使胃液pH值、血清NO浓度、胃组织VEGF质量浓度增加,LPS质量浓度、胃蛋白酶活力降低及胃黏膜抗氧化能力提高有关。

关键词: 燕麦多糖;酒精诱导胃黏膜损伤;损伤指数;氧化应激

Abstract: Objective: The present study aimed to investigate the protective effect of oat polysaccharides on 70% ethanol-induced acute gastric mucosal injury in mice. Methods: Sixty Kunming male mice were randomly divided into normal, model, cimetidine (positive control), and low-, medium- and high-dose oat polysaccharide groups. The positive control group was gavaged with 100 mg/kg mb of cimetidine, and the low-, medium- and high-dose oat polysaccharide groups were intragastrically administered with 100, 200, 400 mg/kg mb of oat polysaccharides, respectively. The administration lasted for 14 consecutive days. On the 15th day, acute gastric mucosal injury was successfully by oral administration of 70% ethanol to all animals except those in the normal group. Afterwards, visceral organ indexes and the degree of gastric mucosal injury were examined and gastric pH, serum nitric oxide (NO) levels, and the levels of interleukin (IL)-10, lipopolysaccharide (LPS), vascular endothelial growth factor (VEGF), malondialdehyde (MDA), glutathione (GSH), pepsin activity and superoxide dismutase (SOD) activity in gastric tissues were measured. Results: Compared with the model group, gastric mucosal injury in the mice treated with oat polysaccharides was significantly reduced, and the most pronounced effect was observed at the high-dose level with an inhibition rate of 76.04%. Furthermore, oat polysaccharides increased the pH of gastric juice, serum NO levels, the activity of SOD and the contents of GSH and VEGF in gastric tissue, and reduced the activity of pepsin and the content of LPS in gastric tissue, especially at the high dose. Conclusion: Oat polysaccharides significantly protect against ethanol-induced acute gastric mucosal injury in mice with the most pronounced effect being observed at the high dose. The mechanism may be related to the increase in the pH of gastric juice, serum NO levels and the content of VEGF in gastric tissue, the decrease in LPS content and pepsin activity, and the enhancement of antioxidant capacity in the gastric mucosa.

Key words: oat polysaccharides; alcohol-induced gastric mucosal injury; damage index; oxidative stress

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