食品科学 ›› 2026, Vol. 47 ›› Issue (7): 174-182.doi: 10.7506/spkx1002-6630-20251005-007

• 营养卫生 • 上一篇    下一篇

基于Caco-2细胞转录组测序解析黄水多糖保护肠道屏障的活性机制

吴紫妍,霍嘉颖,苏建,吴继红,赵东,黄明泉,卢彦坪,郑佳,孙颖,孙宝国   

  1. (1.北京工商大学 中国轻工业酿酒分子工程重点实验室,食品质量与安全北京实验室,北京 100048;2.固态发酵资源利用四川省重点实验室,中国轻工业浓香型白酒固态发酵重点实验室,四川省白酒酿酒专用粮工程技术研究中心,宜宾五粮液股份有限公司,四川 宜宾 644007)
  • 出版日期:2026-04-15 发布日期:2026-05-08
  • 基金资助:
    中国轻工业浓香型白酒固态发酵重点实验室开放基金项目(2023JJ005)

Mechanism of Action of a Polysaccharide Isolated from Huangshui, a Byproduct of Baijiu Fermentation, in Protecting the Intestinal Barrier Identified by Transcriptome Sequencing Based on Caco-2 Cells

WU Ziyan, HUO Jiaying, SU Jian, WU Jihong, ZHAO Dong, HUANG Mingquan, LU Yanping, ZHENG Jia, SUN Ying, SUN Baoguo   

  1. (1. Key Laboratory of Brewing Molecular Engineering of China Light Industry, Beijing Laboratory of Food Quality and Safety, Beijing Technology and Business University, Beijing 100048, China; 2. Key Laboratory of Solid-State Fermentation and Resource Utilization of Sichuan Province, Key Laboratory of Strong Flavor Baijiu Solid-State Fermentation of China Light Industry, Engineering Technology Research Center of Baijiu Brewing Special Grain of Sichuan Province, Wuliangye Yibin Co. Ltd., Yibin 644007, China)
  • Online:2026-04-15 Published:2026-05-08

摘要: 用Caco-2细胞模型,通过转录组测序技术(RNA-seq)探究WLY-0对肠道屏障的保护作用机制。结果表明,WLY-0处理组与脂多糖(损伤对照)处理组之间的差异基因富集于丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路,通过Western blot技术手段,验证WLY-0对MAPK信号通路关键蛋白表达的影响,即添加WLY-0时,p38和Jun氨基末端激酶的磷酸化被显著抑制(P<0.05),细胞外信号相关激酶的磷酸化水平被显著促进(P<0.05),下游促炎症因子IL-6、TNF-α和IL-8的mRNA表达分别降低53.34%、44.56%和37.16%,抑炎因子IL-10和IL-37的mRNA表达分别增加5.96 倍和18.54 倍。本研究确证了WLY-0是通过调节MAPK介导的抗炎通路而改变炎症相关基因,从而抵抗脂多糖对肠道屏障的损伤。该研究为利用黄水多糖制备相关产品辅助治疗炎症性肠病提供了理论依据。

关键词: 黄水多糖;转录组测序技术;肠道屏障;丝裂原活化蛋白激酶信号通路;炎症

Abstract: The aim of this study was to explore the protective mechanism of WLY-0, a polysaccharide extracted from Huangshui, on the intestinal barrier by RNA sequencing (RNA-seq) using the Caco-2 cell model. The results showed that the differential genes between the WLY-0 treatment group and the lipopolysaccharide (LPS)-induced injury group were enriched in the mitogen-activated protein kinase (MAPK) signaling pathway. Subsequently, Western blot was used to verify the effect of WLY-0 on the expression of key proteins in the MAPK signaling pathway. It was found that the addition of WLY-0 significantly inhibited the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) and promoted the phosphorylation of extracellular signalregulated kinase (ERK) (P < 0.05). Meanwhile, the mRNA expression of the downstream pro-inflammatory factors IL-6, TNF-α, and IL-8 decreased by 53.34%, 44.56%, and 37.16%, respectively, while those of the anti-inflammatory factors IL-10 and IL-37 increased by 6.96 and 19.54 times, respectively. These results indicated that WLY-0 protects against LPS-induced intestinal barrier injury by altering the expression of inflammation-related genes through the regulation of the MAPK-mediated anti-inflammatory signaling pathway. This conclusion provides a theoretical basis for developing adjuvant therapeutic products based on Huangshui polysaccharides for inflammatory bowel disease.

Key words: Huangshui polysaccharide; transcriptome sequencing; intestinal barrier; mitogen-activated protein kinase signaling pathway; inflammation

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