Dihydromyricetin alleviates intestinal inflammation by changing intestinal microbial metabolites and inhibiting the expression of the MyD88/NF‐κB signaling pathway
Dihydromyricetin alleviates intestinal inflammation by changing intestinal microbial metabolites and inhibiting the expression of the MyD88/NF‐κB signaling pathway
复制标题
DOI：
10.1002/aro2.21
复制
发表时间：
2023-08
期刊：
影响因子：
--
通讯作者：
Chaoyu Wen;Fan Zhang;Kang Yang;Sufang Han;Shiyan Jian;Baichuan Deng
中科院分区：
文献类型：
--
作者：
Chaoyu Wen;Fan Zhang;Kang Yang;Sufang Han;Shiyan Jian;Baichuan Deng
炎症性肠病（IBD）是人类常见的慢性胃肠道疾病，已成为全球公共卫生挑战。二氢杨梅素（DHM）具有抗炎和抗氧化活性，可以减轻炎症。在这项研究中，我们探讨了DHM对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎和猪空肠上皮细胞（IPEC-J2）暴露于脂多糖（LPS）的影响和潜在机制。我们发现DHM减轻结肠炎小鼠的体重减轻、腹泻和结肠结构损伤。对于肠道微生物，在DHM治疗的结肠炎小鼠中观察到潜在有益菌属的数量显著增加，有害菌属的数量下降。盲肠内容物的代谢组学分析表明，DHM恢复苯丙氨酸代谢，精氨酸生物合成，花生四烯酸代谢紊乱引起的肠道炎症。此外，DHM还降低了LPS处理的IPEC-J2细胞中促炎细胞因子和活性氧的水平。DHM还降低MyD 88和核因子-κB（NF-κB）的表达。总之，我们发现125 mg/kg DHM给药缓解了腹泻，恢复了肠屏障功能，调节了肠道生态失调，并抑制了髓样分化因子88（MyD 88）和NF-κB的表达。因此，DHM可能是IBD的潜在治疗剂。
Inflammatory bowel disease (IBD), a common chronic gastrointestinal disease in humans, has emerged as a global public health challenge. Dihydromyricetin (DHM) has anti‐inflammatory and antioxidant activities, which can alleviate inflammation. In this study, we explored the effect and underlying mechanism of DHM on dextran sulfate sodium (DSS)‐induced colitis in mice and porcine jejunum epithelial cells (IPEC‐J2) exposed to lipopolysaccharide (LPS). We found that DHM alleviated loss of weight, diarrhea, and damage of colon structure in colitis mice. For the intestinal microbial, a significant rise in the amount of the potentially beneficial genera and a decline in the amount of harmful genera were observed in DHM‐treated colitis mice. Metabolomic analysis of cecal content revealed that DHM restored phenylalanine metabolism, arginine biosynthesis, and arachidonic acid metabolism disorders caused by intestinal inflammation. Moreover, DHM decreased the level of pro‐inflammatory cytokines and reactive oxygen species in LPS‐treated IPEC‐J2 cells. DHM also reduced the expression of MyD88 and nuclear factor‐κB (NF‐κB). In summary, we found that 125 mg/kg DHM administration alleviated diarrhea, reinstated intestinal barrier function, modulated intestinal dysbiosis, and suppressed the expression of myeloid differentiation factor 88 (MyD88) and NF‐κB. Therefore, DHM may be a potentially therapeutic agent for IBD.