Abstract
Ulcerative colitis (UC) is considered an immune disease, which is related to the dysbiosis of intestinal microbiota and disorders of the host immune system and metabolism. Sophora flavescens Aiton has been used for the clinical treatment of UC in China and East Asia for thousands of years. It has many traditional prescriptions and modern preparations, and its curative effects are definite. We are the first to report that the flavonoids in Sophora flavescens (S. flavescens) Aiton EtOAc extract (SFE) could potentially attenuate the dextran sodium sulfate–induced UC in mice, which changed the current understanding of considering alkaloids as the only anti-UC pharmacological substances of S. flavescens Aiton. Based on the 16S rRNA gene sequencing and metabolomic analysis, it was found that the anti-UC effects of SFE were due to the regulation of gut microbiota, reversing the abnormal metabolisms, and regulation of the short-chain fatty acids synthesis. Notably, according to the interaction networks of specific bacteria and “bacteria and metabolites” co-expression network, the SFE could enrich the abundance of the commensal bacterium Lactobacillus, Roseburia, norank_f__Muribaculaceae, Anaerotruncus, Candidatus_Saccharimona, and Parasutterella, which are proposed as potentially beneficial bacteria, thereby playing vital roles in the treatment of UC.
Highlights
Ulcerative colitis (UC) is considered an immune disease, in which lesions mainly occur in the sigmoid colon and rectum, which are manifested by the inflammatory infiltration and injury of colonic mucosa
Chemicals and Reagents In October 2017, fresh Sophora flavescens (S. flavescens) Aiton root samples were harvested from the planting base of S. flavescens Aiton GAP in Chinese medicinal materials of Shanxi Zhendong Pharmaceutical Co., Ltd; Mesalazine was purchased from Heilongjiang Sunflower Pharmaceutical Group’s Jiamusi Luling Pharmaceutical Co., Ltd; dextran sulfate sodium (DSS), benzidine, 3% H2O2, and chromatography grade ethyl acetate were purchased from Shanghai Macklin Biochemical Technology Co., Ltd; chromatography grade acetonitrile and formic acid were purchased from Thermo Scientific Co., Ltd; primary antibodies: IL-1β, IL-6, IL-10, TNF-α, COX-2, GADPH, and inducible nitric oxide synthase (iNOS) and secondary antibodies were purchased from Affinity Biosciences Co., Ltd; Kolliphor P 188 co-solvent was brought from BASF SE Co., Ltd; Distilled water was purchased from
MOBIO PowerSoil DNA Isolation Kit was purchased from MOBIO Co., Ltd; TransStart FastPfu DNA Polymerase was purchased from TransGen Biotech Co., Ltd; TM Quant-iT Broad-Range DNA Assay Kit and primer were purchased from Invitrogen Co., Ltd; agarose was purchased from Guangzhou Haoma Biological Technology Co., Ltd; superoxide dismutase (SOD), myeloperoxidase (MPO), and malondialdehyde (MDA) kits were purchased from Nanjing Jiancheng Bioengineering Institute; AxyPrep DNA Gel Extraction Kit was purchased from Axygen Co., Ltd; 2methylvaleric acid was purchased from ChengduChromaBiotech Co., Ltd; anhydrous sodium sulfate and sodium chloride powder were purchased from Beijing Yinuokai Technology Co., Ltd
Summary
Ulcerative colitis (UC) is considered an immune disease, in which lesions mainly occur in the sigmoid colon and rectum, which are manifested by the inflammatory infiltration and injury of colonic mucosa. UC has a complex pathogenesis, which is attributed to the genetics, diet, immune abnormalities, and dysbiosis of intestinal microbiota (Liu and Stappenbeck, 2016; Ungaro et al, 2017; Khan et al, 2020). The changes in immunity, metabolism, and mucosal structure, caused by the “host–microbe” interaction, are the driving forces of UC. In UC, the diversity of intestinal microbiota and abundance of short-chain fatty acids (SCFAs)–producing and aromatic hydrocarbon receptors (AhRs)–producing bacteria decreased while that of the mucus-degrading and pathogenic bacteria increased, which caused changes in metabolites, such as butyric acid and 2-indolecarboxylic acid; the changes in these metabolites reduced their protective effect on the intestinal mucosa and affected the balance of Th and Treg cells, thereby accelerating the destruction of colonic mucosa and developing UC (Agus et al, 2018; Natividad et al, 2018; Nascimento et al, 2020). Finding of drugs based on the regulation of “host–microbe” interaction might provide a novel therapeutic strategy for the treatment of UC
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