Baitouweng Decoction Alleviates Dextran Sulfate Sodium–Induced Ulcerative Colitis Through Nrf2/HO-1 Pathway Activation and HMGB1 Downregulation

crossref(2021)

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摘要
Abstract BackgroundThe phrase “baitouweng (BTW) decoction” was first recorded in the ancient Chinese medical text Shang Han Za Bing Lun. BTW decoction has been widely used by practitioners of (traditional) Chinese medicine.[VN1] It has been used to treat ulcerative colitis (UC) for hundreds of years. In this study, we investigated the antioxidative properties of BTW and the intestinal immunity of mice with dextran sulfate sodium (DSS)–induced UC and further investigated the mechanism by which BTW alleviates UC.MethodsUC was induced in mice by using DSS. The mice were randomly divided into the following five groups: control, DSS, BTW (5, 10, and 20 g/kg[VN2] ), berberine (BBR), and 5-aminosalicylic acid (5-ASA). Except for the control group, 3% DSS was administered in drinking water to all groups for 7 days, and and the other groups were intragastrically administered with BTW(5, 10, and 20 g/kg)、BBR and 5-ASA independently.[VN3] After gavaging for 12 days, the mice were killed. Subsequently, body weight loss, colon length, colon histopathology, inflammatory cytokine expression, and intestinal protein expression were measured.ResultsBTW effectively reduced the symptoms and histopathological scores of UC mice. Additionally, it downregulated the inflammatory factors interleukin (IL)-6 and IL-1β, the immunoglobulins vascular cell adhesion molecule 1 and intercellular adhesion molecule 1, and metalloprotease matrix metallopeptidase 9. Moreover, it downregulated high mobility group box 1 protein. Furthermore, it inhibited the nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.ConclusionBTW considerably alleviated the inflammatory symptoms of mice with acute colitis, and the latent mechanism of BTW may be related to various signaling pathways, including the modulation of antioxidant signaling pathways such as the Nrf2/HO-1 pathway.
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