Costunolide improved dextran sulfate sodium-induced acute ulcerative colitis in mice through NF-κB, STAT1/3, and Akt signaling pathways

2020 ◽  
Vol 84 ◽  
pp. 106567 ◽  
Author(s):  
Fan Xie ◽  
Hai Zhang ◽  
Chuan Zheng ◽  
Xiao-fei Shen
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathways ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Akt Signaling

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

2021 ◽  
Author(s):  
Weina Zhu ◽  
Chunhua Ma ◽  
Fuqiong Zhou ◽  
Jie Ruan ◽  
Yajie Zhang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Aminosalicylic Acid

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.

scholarly journals Dihydroartemisinin Protects against Dextran Sulfate Sodium-Induced Colitis in Mice through Inhibiting the PI3K/AKT and NF-κB Signaling Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Ning Li ◽  
Wenjing Sun ◽  
Xin Zhou ◽  
Hao Gong ◽  
Yuqing Chen ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathways ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Body Weight Loss ◽  
Intestinal Epithelial ◽  
Histological Damage ◽  
Inflammatory Bowel

Ulcerative colitis is a common inflammatory bowel disease, and the activation of thePI3K/AKT and NF-κB signaling pathways plays a pivotal role in its pathogenesis. Dihydroartemisinin (DHA) is a widely used antimalarial drug and has shown anticancer effect partially through inhibiting the activation of PI3K/AKT and NF-κB. This study aimed to investigate the effect of dihydroartemisinin on ulcerative colitis and its mechanism. Adult male C57 mice were subjected to 3.0% dextran sulfate sodium (DSS) for seven days; simultaneously, dihydroartemisinin or control saline was administered by oral gavage once a day. In vitro, the intestinal epithelial cell-6 was treated with LPS for 24 hours with or without dihydroartemisinin combined with PI3K/Akt activator 740 Y-P or NF-κB activator phorbol myristate acetate. Western blotting was used to test the activation of PI3K/AKT and NF-κB. Dihydroartemisinin significantly ameliorated body weight loss, shortened colon length, and increased DAI in DSS-induced colitis. Meanwhile, histological damage was improved and was accompanied by decreased expression and secretion of proinflammatory cytokines. Moreover, DSS-induced elevation of phosphorylation of PI3K, AKT, IKKα, IκBα, and NF-κB (p65) was remarkably blunted by dihydroartemisinin both in vivo and in vitro, indicating an inhibitive property on the PI3K/AKT and NF-κB signaling pathways. Furthermore, administration of 740 Y-P or PMA significantly blocked protective activity of dihydroartemisinin against colitis in vitro. In conclusion, dihydroartemisinin can attenuate DSS-induced colitis, and its anticolitis effect might be mediated via the PI3K/AKT and NF-κB signaling pathways. DHA might serve as a promising drug for patients with ulcerative colitis.

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

2015 ◽  
Vol 6 (11) ◽  
pp. 3454-3463 ◽  
Author(s):  
Bo Liu ◽  
Qinlu Lin ◽  
Tao Yang ◽  
Linna Zeng ◽  
Limin Shi ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Α

Oral administration of oat β-glucan ameliorates DSS induced colitis in mice by decreasing the expression of inflammatory cytokines TNF-α, IL-1β, IL-6 and iNOS.

Anti-Colitic Effects of Herbal Medicine HPL-01 on Dextran Sulfate Sodium Induced Ulcerative Colitis in Rat

2021 ◽  
Vol 35 (2) ◽  
pp. 64-70
Author(s):  
Hyoung-Kwon Jo ◽  
Dae-Sung Kim ◽  
Seong-Wan Cho ◽  
Na-Rae Shin ◽  
Young Mi Park ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Herbal Medicine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

CD39/CD73/A2a Adenosine Metabolic Pathway: Targets for Moxibustion in Treating DSS-Induced Ulcerative Colitis

2021 ◽  
Vol 49 (03) ◽  
pp. 661-676
Author(s):  
Yuanbing Zhu ◽  
Zhiqi Zhuang ◽  
Qiaofeng Wu ◽  
Sirui Lin ◽  
Na Zhao ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Animal Experiments ◽  
Treg Cells ◽  
Colonic Tissue ◽  
Colonic Epithelial Cells ◽  
A2a Receptor ◽  
Draining Lymph Nodes

Ulcerative Colitis (UC) is a chronic inflammation disease, and the incidence of UC is increasing recently. Both clinical trials and animal experiments show that moxibustion is a complementary and alternative treatment for UC. Previous studies showed that moxibustion can improve UC by regulating the balance of Tregs and Th17 (Sun et al., 2017). Treg cells is one subset of CD4[Formula: see text] T cells that exert the immunosuppressive function. CD39 and CD73, expressed on the surface of Tregs, hydrolyze ATP to AMP and are further involved in the immunosuppressive function of Tregs. In this study, we investigated the effect of moxibustion on CD39[Formula: see text] Tregs and CD73[Formula: see text] Tregs in dextran sulfate sodium (DSS) induced UC mice. The A2a receptor (A2aR), one of the targets of adenosine, was also detected. The results showed that moxibustion could increase the expression of CD39, CD73, and A2aR in colonic tissue and improve the proportion of CD39[Formula: see text] Tregs and CD73[Formula: see text] Tregs in peripheral blood, inguinal draining lymph nodes and spleen in the UC model. Additionally, A2aR agonists enhanced the cell viability of colonic epithelial cells and inhibit the production of cytokines IL-6 and TNF-[Formula: see text] in vitro, which may further influence the pathway of ATP purine signal metabolism and alleviates the gut inflammation of UC mice. Taken together, this study provides supplemental evidence to reveal the immune related mechanism of moxibustion in the treatment of UC.

Desmethylbellidifolin Attenuates Dextran Sulfate Sodium-Induced Colitis: Impact on Intestinal Barrier, Intestinal Inflammation and Gut Microbiota

Planta Medica ◽  
2021 ◽  
Author(s):  
Jiaqi Wu ◽  
Yuzheng Wu ◽  
Yue Chen ◽  
Mengyang Liu ◽  
Haiyang Yu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Activity Index ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Function Evaluation ◽  
Biological Drugs

AbstractUlcerative colitis has been recognized as a chronic inflammatory disease predominantly disturbing the colon and rectum. Clinically, the aminosalicylates, steroids, immunosuppressants, and biological drugs are generally used for the treatment of ulcerative colitis at different stages of disease progression. However, the therapeutic efficacy of these drugs does not satisfy the patients due to the frequent drug resistance. Herein, we reported the anti-ulcerative colitis activity of desmethylbellidifolin, a xanthone isolated from Gentianella acuta, in dextran sulfate sodium-induced colitis in mice. C57BL/6 mice were treated with 2% dextran sulfate sodium in drinking water to induce acute colitis. Desmethylbellidifolin or balsalazide sodium was orally administrated once a day. Biological samples were collected for immunohistological analysis, intestinal barrier function evaluation, cytokine measurement, and gut microbiota analysis. The results revealed that desmethylbellidifolin alleviated colon shortening and body weight loss in dextran sulfate sodium-induced mice. The disease activity index was also lowered by desmethylbellidifolin after 9 days of treatment. Furthermore, desmethylbellidifolin remarkably ameliorated colonic inflammation through suppressing the expression of interleukin-6 and tumor necrosis factor-α. The intestinal epithelial barrier was strengthened by desmethylbellidifolin through increasing levels of occludin, ZO-1, and claudins. In addition, desmethylbellidifolin modulated the gut dysbiosis induced by dextran sulfate sodium. These findings suggested that desmethylbellidifolin effectively improved experimental ulcerative colitis, at least partly, through maintaining intestinal barrier integrity, inhibiting proinflammatory cytokines, and modulating dysregulated gut microbiota.

Sign in / Sign up

Export Citation Format

Share Document