文献类型：期刊文献

英文题名：Sishen Wan Treats Ulcerative Colitis in Rats by Regulating Gut Microbiota and Restoring the Treg/Th17 Balance

作者：Wang, Yingyun[1];Zhu, Xiangdong[2];Liang, Yonglin[1];Li, Xinze[3];Wang, Yan[2];Li, Jie[1]

第一作者：王圆圆;王媛媛;汪元元

通信作者：Zhu, XD[1];Wang, Y[1]

机构：[1]Gansu Univ Chinese Med, Lanzhou 730000, Peoples R China;[2]Ningxia Med Univ, Yinchuan 750004, Peoples R China;[3]Tianjin Univ Tradit Chinese Med, Tianjin 301617, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Ningxia Med Univ, Yinchuan 750004, Peoples R China.

年份：2022

卷号：2022

外文期刊名：EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE

收录：;Scopus(收录号：2-s2.0-85146087466);WOS:【SCI-EXPANDED(收录号:WOS:000908911600001)】；

基金：AcknowledgmentsThis work was supported by the National Natural Science Foundation of China (Grant no. 81960826) and Graduate Innovation Fund of Gansu University of Chinese Medicine (Grant no. 2021CX39).

语种：英文

摘要：Objective. This study was aimed to explore the mechanism of Sishen Wan (SSW) in treating ulcerative colitis (UC) in a rat model of spleen-kidney yang deficiency pattern by regulating gut microbiota and the content of butyric acid in short-chain fatty acid (SCFAs) and restoring regulatory T (Treg)/T helper type 17 (Th17) balance from the perspective of the correlation between gut microbiota and immune function. Methods. The UC rat model of spleen-kidney yang deficiency pattern was established by the method of combining disease and syndrome (intragastric administration of senna leaf, subcutaneous injection of hydrocortisone, and enema with 2,4-dinitrobenzenesulfonic acid (DNBS)/ethanol solution). After successful modeling, rats were randomly divided into six groups: the blank group, model group, low-, middle-, and high-dose Sishen Wan groups, and mesalazine group. Samples were taken after continuous administration for 3 weeks. The general conditions and body weight of the rats were observed and recorded, and the disease activity index (DAI) score was calculated. Colonic mucosal injury was observed, and a colonic mucosal damage index (CMDI) score was calculated. Histopathological changes in colon tissues were determined by hematoxylin and eosin (H&E) staining, and the histopathological score (HS) was calculated. The serum levels of transforming growth factor-beta 1 (TGF-beta 1), interleukin (IL)-6, IL-10, and IL-17 were determined by enzyme-linked immunosorbent assay (ELISA) assays. The expression of TGF-beta 1, signal transducer and activator of transcription 3 (STAT3), and peroxisome proliferator-activated receptor gamma (PPAR gamma) was determined by Western blot analysis. The proportion of Th17 and Treg cells in colon tissue was determined by flow cytometry. The relative abundance of gut microbiota was determined by 16S rDNA sequencing, and the concentration of butyric acid of SCFAs was determined by gas chromatography-mass spectrometry (GC-MS). Results. Administration of SSW significantly improved the pathological changes of colon tissue in UC rats and could attenuate the DAI and CMDI scores, and the HS. SSW significantly decreased the serum levels of IL-6 and IL-17 and increased the serum levels of TGF-beta 1 and IL-10. In addition, SSW increased the expression of TGF-beta 1 and PPAR gamma and decreased the expression of STAT3 in colon tissue in a dose-dependent manner. Furthermore, SSW significantly decreased the proportion of Th17 cells and increased the proportion of Treg cells in colon tissue. Additionally, SSW altered the gut microbiota, including an increase in the relative abundance of Firmicutes and a decrease in Bacteroidota at the phylum level and an increase in the relative abundance of Lactobacillus at the genus level. Moreover, SSW significantly increased the concentration of butyric acid. Conclusions. Combined, these data suggested that SSW increased the relative abundance of firmicutes and the level of butyric acid and restored the balance of Treg/Th17 immune axis and gut homeostasis, thus delaying the progress of UC.