Yang Suqin, Huang Jingtao, Tan Wenjing, Xia Xiankun, Gan Dali, Ren Yalei, Su Hanwen, Xiang Meixian
School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan, 430074, Hubei, People's Republic of China.
Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, People's Republic of China.
Nat Prod Bioprospect. 2024 Aug 12;14(1):44. doi: 10.1007/s13659-024-00468-6.
Xiaoyankangjun tablet (XYKJP) is a traditional Chinese medicine formulation used to treat intestinal disorders in clinical practice. However, the specific therapeutic mechanism of action of XYKJP in colitis has not yet been elucidated. This study aimed to reveal the multifaceted mechanisms of action of XYKJP in treating colitis. The model established based on DSS-induced colitis in C57BL/6 mice was employed to estimate the effect of XYKJP on colitis, which was then followed by histological assessment, 16S rRNA sequencing, RT-qPCR, ELISA, and Western blot. XYKJP alleviated the symptoms of DSS-induced colitis mainly by reducing oxidative stress, inflammatory responses, and intestinal mucosal repair in colitis tissues. In addition, XYKJP regulated the intestinal flora by increasing the relative abundance of Akkermansia and Bifidobacterium and reducing the relative abundance of Coriobacteriaceae_UCG-002. Mechanistically, XYKJP increased the content of short-chain fatty acids (SCFAs) in the feces, particularly propanoic acid and butyric acid, activated their specific receptor GPR43/41, furthermore activated the Nrf2/HO-1 pathway, and suppressed the JAK2/STAT3 pathway. XYKJP significantly alleviated the symptoms of experimental colitis and functioned synergistically by regulating the intestinal flora, increasing the production of SCFAs, and activating their specific receptors, thereby repressing oxidative stress and inflammation.
消炎抗菌片(XYKJP)是一种在临床实践中用于治疗肠道疾病的中药制剂。然而,XYKJP在结肠炎中的具体治疗作用机制尚未阐明。本研究旨在揭示XYKJP治疗结肠炎的多方面作用机制。采用基于DSS诱导的C57BL/6小鼠结肠炎模型来评估XYKJP对结肠炎的影响,随后进行组织学评估、16S rRNA测序、RT-qPCR、ELISA和蛋白质印迹分析。XYKJP主要通过减轻结肠炎组织中的氧化应激、炎症反应和促进肠黏膜修复来缓解DSS诱导的结肠炎症状。此外,XYKJP通过增加阿克曼氏菌和双歧杆菌的相对丰度以及降低柯里杆菌科_UCG-002的相对丰度来调节肠道菌群。从机制上讲,XYKJP增加了粪便中短链脂肪酸(SCFAs)的含量,特别是丙酸和丁酸,激活了它们的特异性受体GPR43/41,进而激活了Nrf2/HO-1通路,并抑制了JAK2/STAT3通路。XYKJP显著减轻了实验性结肠炎的症状,并通过调节肠道菌群、增加SCFAs的产生和激活它们的特异性受体发挥协同作用,从而抑制氧化应激和炎症。