实验方法与实验动物 EXPERIMENTAL METHOD AND ANIMAL

甘露寡糖对阿司匹林诱导大鼠肠道损伤修复作用的研究

  • 陈勇江 ,
  • 王金荣 ,
  • 乔汉桢 ,
  • 苏兰利 ,
  • 唐桂芬 ,
  • 黄进 ,
  • 赵银丽 ,
  • 高温婷
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  • 1. 河南工业大学生物工程学院, 郑州 450001;
    2. 河南牧业经济学院, 郑州 450011
陈勇江(1995-),男,河南新乡人,硕士研究生,研究方向为动物营养和饲料科学专业。E-mail:1559899363@qq.com

收稿日期: 2020-11-13

  网络出版日期: 2021-06-10

基金资助

国家自然科学基金资助项目(U1604106,31702235)

Effects of Mannose Oligosaccharide on Repair of Intestinal Injury Induced by Aspirin in Rats

  • CHEN Yongjiang ,
  • WANG Jinrong ,
  • QIAO Hanzhen ,
  • SU Lanli ,
  • TANG Guifen ,
  • HUANG Jin ,
  • ZHAO Yinli ,
  • GAO Wenting
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  • 1. College of Bioengineering, Henan University of Technology, Zhengzhou 450001, China;
    2. Henan University of Animal Husbandry and Economy, Zhengzhou 450011, China

Received date: 2020-11-13

  Online published: 2021-06-10

摘要

本试验旨在研究甘露寡糖(MOS)对阿司匹林(ASA)诱导大鼠的肠道损伤修复作用。试验采用单因素试验设计,选用36只6周龄150~180 g大鼠,经过1周适应性饲养后随机分为6组,每组6只,单笼饲养。空白组灌胃生理盐水,模型组灌胃2周200 mg/kg ASA后灌胃1周生理盐水,MOS组灌胃1周生理盐水后灌胃2周600 mg/kg MOS,ASA1、ASA2和ASA3组分别灌胃2周50、100和200 mg/kg ASA后灌胃1周600 mg/kg MOS。结果表明:与空白组相比,ASA1组血清白细胞介素-2(IL-2)含量及溶菌酶(LZM)、总超氧化物歧化酶(T-SOD)活性和肠道隐窝深度(CD)无显著差异(P>0.05),ASA2组血清IL-2含量和CD无显著差异(P>0.05);ASA3组血清T-SOD活性较模型组显著升高(P<0.05),但是与空白组仍存在显著差异(P<0.05),但肠道绒毛高度与隐窝深度比值(VH/CD)较模型组显著升高(P<0.05),且与空白组不存在显著差异(P>0.05)。与空白组相比,模型组黏膜分泌型免疫球蛋白A(sIgA)含量减少了30.32%(P<0.05),ASA1组不存在显著差异(P>0.05),ASA2和ASA3组分别降低了7.39%和12.50%(P<0.05);与模型组相比,ASA3组升高了25.59%(P<0.05)。在本试验条件下,600 mg/kg的MOS对低浓度ASA诱导的大鼠肠道损伤有较好的修复效果,提高了ASA1组大鼠血清中IL-2含量和LZM活性及sIgA含量,改善肠道绒毛结构,提高CD和VH/CD;与模型组相比,MOS促进了ASA3组大鼠肠道发育并提高了血清T-SOD活性。

本文引用格式

陈勇江 , 王金荣 , 乔汉桢 , 苏兰利 , 唐桂芬 , 黄进 , 赵银丽 , 高温婷 . 甘露寡糖对阿司匹林诱导大鼠肠道损伤修复作用的研究[J]. 动物营养学报, 2021 , 33(6) : 3523 -3531 . DOI: 10.3969/j.issn.1006-267x.2021.06.054

Abstract

The objective of the experiment was to investigate the therapeutic effect of mannose oligosaccharides (MOS) on repairmen of aspirin (ASA) induced intestinal injury in rats. The experiment was designed by single factor test, 36 rats at 6 weeks of age with body weight of 150 to 180 g were randomly divided into 6 groups after 1 week adaptive feeding, each group had 6 rats which fed in a single cage. The model group was administered orally 200 mg/kg ASA for 2 weeks then saline for 1 week. The MOS group was administered orally 600 mg/kg MOS. The ASA1, ASA2 and ASA3 groups were administered orally 50, 100 and 200 mg/kg ASA, respectively, then 600 mg/kg MOS for the next week. The blank group received the same amount of normal saline. The results showed that compared with the blank group, there was no significant difference in interleukin-2 (IL-2) content, lysozyme (LZM) and total superoxide dismutase (T-SOD) activities and intestinal crypt depth (CD) in ASA1 group (P>0.05), no significant difference in IL-2 content and CD in ASA2 group and control group (P>0.05) and ASA3 group was higher than model group (P<0.05), the ratio of villi height to crypt depth (VH/CD) was higher than that in model group (P<0.05), and there was no difference from the blank group (P>0.05). Compared with blank group, the content of mucosal secretarial immunoglobulin A (sIgA) in model group was decreased by 30.32% (P<0.05), but there was no significant difference from ASA1 group (P>0.05), and it was decreased by 7.39% and 12.50% in ASA2 and ASA3 groups, respectively (P<0.05). Compared with model group, it was increased by 25.59% in ASA3 group (P<0.05). The present study is demonstrated that 600 mg/kg MOS administered orally to the rats with intestinal injury which induced by low concentration of ASA can improve the rats intestinal morphology, increase intestinal CD and VH/CD, and increase the serum IL-2 content and LZM activity and sIgA content in rats in ASA1 group, MOS can promote intestinal development and increase serum T-SOD activity in the ASA3 group compared with the model group.

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