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.

Neferine, a Bisbenzylisoquinoline Alkaloid, Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis

2018 ◽  
Vol 46 (06) ◽  
pp. 1263-1279 ◽  
Author(s):  
Xiaxia Wu ◽  
Yanling Guo ◽  
Xiangjing Min ◽  
Lixia Pei ◽  
Xiuping Chen
Keyword(s):  
Ulcerative Colitis ◽  
Protein Expression ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Biological Activities ◽  
Necrosis Factor Alpha ◽  
Cox 2 ◽  
Anti Inflammatory

Both the incidence and prevalence of ulcerative colitis (UC) are increasing throughout the world. Neferine, a natural alkaloid, demonstrated a variety of biological activities. In this study, the anti-inflammatory effect of neferine was investigated. Raw264.7 cells were stimulated with lipopolysaccharide (LPS) or LPS plus Z-VAD-fmk (Z-VAD). The inhibitory effect of neferine on secretion of nitrite, cytokines tumor necrosis factor alpha (TNF-[Formula: see text]) and interleukin 6 (IL-6), expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was determined. The protective effect of neferine was investigated in dextran sulfate sodium (DSS)-induced UC mouse model. Neferine significantly inhibited LPS and LPS plus Z-VAD induced secretion of nitrite, cytokines, and expression of iNOS and COX-2. Oral administration of neferine (10[Formula: see text]mg/kg and 25[Formula: see text]mg/kg) significantly reduced DSS-induced mouse weight loss, decreased disease activity index (DAI) scores, improved colon pathological changes, and decreased plasma cytokines. In addition, neferine significantly inhibited the protein expression of iNOS, COX-2, receptor-interacting protein 1 (RIP1), RIP3, mixed lineage kinase domain-like protein (MLKL), and increased the protein expression of caspase-8 in colon tissues. These data suggest that neferine was a potent anti-inflammatory agent against LPS and DSS induced inflammation both in vitro and in vivo.

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.

scholarly journals Intestinal mesenchymal cells regulate immune responses and promote epithelial regeneration in vitro and in dextran sulfate sodium‐induced experimental colitis in mice

2021 ◽  
Author(s):  
Laura Hidalgo‐Garcia ◽  
José Alberto Molina‐Tijeras ◽  
Francisco Huertas‐Peña ◽  
Antonio Jesús Ruiz‐Malagón ◽  
Patricia Diez‐Echave ◽  
...  
Keyword(s):  
Immune Responses ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Experimental Colitis ◽  
Mesenchymal Cells ◽  
Epithelial Regeneration ◽  
Regeneration In Vitro

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

scholarly journals The protective effect of curcumin on rats with DSS-induced ulcerative colitis and its mechanisms

2021 ◽  
Author(s):  
Jing Guo ◽  
Yan-yan Zhang ◽  
Mei Sun ◽  
Ling-fen Xu
Keyword(s):  
Ulcerative Colitis ◽  
Th17 Cells ◽  
Dextran Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Treg Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
T Helper ◽  
T Helper 17 ◽  
Inflammatory Bowel

Abstract Aim This study aimed to explore effect of curcumin on inflammatory bowel disease (IBD) in rats and its mechanism.Methods: A dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) rat model was established. The disease activity index (DAI) scores were calculated. The histopathological damage scores were determined by haematoxylin-eosin (H&E) staining. Regulatory T (Treg) cells and T helper 17 (Th17) cells in the spleen were analysed by flow cytometry. The levels of interleukin (IL)-10 and IL-17A were determined by enzyme-linked immunosorbent assay (ELISA). Results: Compared with the DSS model group, the curcumin group exhibited significantly reduced DAI scores and improvements in histopathological damage. The expression of CD4+IL-17+ Th17 cells was significantly lower and the expression of CD4+CD25+Foxp3+ Treg cells was significantly higher in the curcumin group than in the DSS group.Conclusion: Curcumin may be a new and effective treatment for IBD by regulating the balance of Treg/Th17 cells and the expression of IL-10 and IL-17A.

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