CP ‐25 exerts therapeutic effects in mice with dextran sodium sulfate‐induced colitis by inhibiting GRK2 translocation to downregulate the TLR4‐NF‐κB‐NLRP3 inflammasome signaling pathway in macrophages

IUBMB Life ◽  
2021 ◽  
Author(s):  
Ying Li ◽  
Meng‐Ya Jiang ◽  
Jing‐Yu Chen ◽  
Zhou‐Wei Xu ◽  
Jia‐Wei Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate ◽  
Therapeutic Effects

Therapeutic Effects of Ecabet Sodium, an Antiulcer Drug, on Dextran Sodium Sulfate–Induced Ulcerative Colitis in Rats

2005 ◽  
Vol 50 (5) ◽  
pp. 922-927 ◽  
Author(s):  
Tsunehisa Noto ◽  
Hiroshi Yamada ◽  
Takashi Inui ◽  
Kayoko Okuyama ◽  
Ayako Watanable ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate ◽  
Therapeutic Effects ◽  
Antiulcer Drug ◽  
Ecabet Sodium

scholarly journals The Influence of Ghrelin on the Development of Dextran Sodium Sulfate-Induced Colitis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Aleksandra Matuszyk ◽  
Dagmara Ceranowicz ◽  
Zygmunt Warzecha ◽  
Piotr Ceranowicz ◽  
Krzysztof Fyderek ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Sodium Sulfate ◽  
Colonic Mucosa ◽  
Body Weight Gain ◽  
Interleukin 1 ◽  
Mucosal Damage ◽  
Dextran Sodium Sulfate ◽  
Therapeutic Effects ◽  
Preventive Effect ◽  
Effect Of Treatment

Ghrelin has protective and therapeutic effects in the gut. The aim of present studies was to investigate the effect of treatment with ghrelin on the development of colitis evoked by dextran sodium sulfate (DSS). Methods. Studies have been performed on rats. Colitis was induced by adding 5% DSS to the drinking water for 5 days. During this period animals were treated intraperitoneally twice a day with saline or ghrelin given at the dose of 8 nmol/kg/dose. On the sixth day, animals were anesthetized and the severity of colitis was assessed. Results. Treatment with ghrelin during administration of DSS reduced the development of colitis. Morphological features of colonic mucosa exhibited a reduction in the area and deep of mucosal damage. Ghrelin reversed the colitis-induced decrease in blood flow, DNA synthesis, and superoxide dismutase activity in colonic mucosa. These effects were accompanied by a decrease in the colitis-evoked increase in mucosal concentration of interleukin-1β and malondialdehyde. Treatment with ghrelin reversed the DSS-induced reduction in body weight gain. Conclusions. Administration of ghrelin exhibits the preventive effect against the development of DSS-induced colitis. This effect seems to be related to ghrelin’s anti-inflammatory and antioxidative properties.

scholarly journals A comparative analysis of NLRP3-related inflammatory mediators in synovial fluid in temporomandibular joint osteoarthritis and internal derangement

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mengying Jia ◽  
Yaoguang Lv ◽  
Yingjie Xu ◽  
Zhongcheng Gong
Keyword(s):  
Synovial Fluid ◽  
Temporomandibular Joint ◽  
Signaling Pathway ◽  
Inflammatory Mediators ◽  
Nlrp3 Inflammasome ◽  
Internal Derangement ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Clinical Effects ◽  
Temporomandibular Joint Osteoarthritis

Abstract Background The nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome signaling pathway is a highlighted topic in the field of inflammation. However, there is little research on the relationship between the NLRP3 inflammasome pathway and temporomandibular joint osteoarthritis (TMJOA). The aim of this study was to examine the expression of inflammatory mediators related to the NLRP3 inflammasome in the synovial fluid of patients with condylar cartilage degeneration and verify the clinical effects of sodium hyaluronic acid (HA) treatment on TMJOA. Methods Patients diagnosed with temporomandibular joint internal derangement (TMJID) without condylar defects and TMJOA with condylar defects were divided into two groups. There were thirty patients in each group, and inflammatory mediators related to the NLRP3 inflammasome, including interleukin-1 beta (IL-1β), IL-18, NLRP3, and cysteinyl aspartate specific proteinase 1 (CASP1), in synovial fluid were measured by enzyme-linked immunosorbent assay (ELISA). Eighteen patients in the TMJOA group were retested after two HA treatments to evaluate the therapeutic effects of HA. Results IL-1β, IL-18, NLRP3 and CASP1 were all positive in the two groups, and TMJOA patients with condylar defects had higher expression of these molecules than TMJID patients (P < 0.05). IL-1β, IL-18, and NLRP3 were decreased after two HA treatments (P<0.05), but there was no significant difference in CASP1 after two HA injections (P = 0.549). Conclusions The NLRP3 inflammasome signaling pathway may be involved in condylar degeneration. HA could reduce some inflammatory molecules to alleviate inflammation.

scholarly journals MiR-223 improves intestinal inflammation through inhibiting the IL-6/STAT3 signaling pathway in dextran sodium sulfate-induced experimental colitis

2020 ◽  
Author(s):  
Juanjuan Zhang ◽  
Chenyang Wang ◽  
Zhen Guo ◽  
Binlin Da ◽  
Weiming Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Sodium Sulfate ◽  
Quantitative Polymerase Chain Reaction ◽  
Negative Control ◽  
Dextran Sodium Sulfate ◽  
Enzyme Linked Immunosorbent Assay ◽  
Colonic Inflammation ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Tnf Α

Abstract Background: The pathogenesis of inflammatory bowel disease (IBD) has not yet been clarified and is closely related to several proinflammatory factors. MicroRNA-233 (miR-223) might be involved in the development of IBD; however, the mechanism underlying its pathogenesis is unclear. In this study, we attempted to determine the role of miR-223 in dextran sodium sulfate (DSS)-induced colitis and explore the involvement of the IL-6/STAT3 pathway in the development of intestinal mucosal inflammation.Methods: Male C57BL/6 mice were divided into six groups: control (WT) group, DSS group, DSS+miR-223 agomir (DSS+A) group, DSS+miR-223 agomir negative control (DSS+A+NC) group, DSS+miR-223 antagomir (DSS+AN) group and DSS+miR-223 antagomir negative control (DSS+AN+NC) group. Body weight, stool consistency, fecal blood and the disease activity index (DAI) score were recorded daily. The length of each colon was measured, and colonic inflammation was evaluated with hematoxylin and eosin (H&E) staining and histopathological scoring. The expression of myeloperoxidase (MPO), TNF-α, IL-6, IL-10 and IL-17 in the colonic tissues was measured by Enzyme-linked Immunosorbent Assay (ELISA) and real-time quantitative polymerase chain reaction (RT-qPCR). The mRNA expression of gp130, Bcl-2 and Bcl-xl in the colon was measured using RT-qPCR. The colonic levels of STAT3 and p-STAT3 were determined by Western blotting.Results: MiR-223 expression in the terminal ileum and colon was increased in the DSS group compared with the WT group. Colitis symptoms were significantly alleviated in the DSS+A group and exacerbated in the DSS+AN group after administration of the miR-223 agomir and antagomir, respectively. MPO, TNF-α, IL-6 and IL-17 were decreased and IL-10 was increased in the DSS+A group, but these changes were reversed in the DSS+AN group. Gp130 mRNA, p-STAT3, Bcl-2 and Bcl-xl in the colon declined in the DSS+A group, but these levels increased in the DSS+AN group.Conclusion: The upregulation of miR-223 by agomir administration alleviated colonic inflammation in a DSS-induced colitis model, which was likely mediated by inhibiting the production of proinflammatory cytokines via the IL-6/STAT3 signaling pathway. These findings provide evidence that miR-223 might have potential therapeutic implications in IBD.

scholarly journals Ginseng Polysaccharides and its Effective Subfraction Protects Against Dextran Sodium Sulfate-Induced Colitis via Regulating NF-κB Signaling Pathway, Recovering Intestinal Barrier and Adjusting Gut Microbiota

2021 ◽  
Author(s):  
Shanshan Li ◽  
Yuli Qi ◽  
Duoduo Ren ◽  
Yue Zhang ◽  
Yinshi Sun
Keyword(s):  
Gut Microbiota ◽  
Signaling Pathway ◽  
Sodium Sulfate ◽  
Intervention Strategy ◽  
Intestinal Barrier ◽  
Dextran Sodium Sulfate ◽  
Signalling Pathway ◽  
Ginseng Polysaccharide ◽  
Acidic Fraction ◽  
Related Proteins

Abstract Background: Polysaccharides from Panax ginseng is a natural carbohydrates with multiple activities. Our previous work found that ginseng polysaccharide could recover the gut microbiota dysbiosis caused by antibiotic. However, it was little known about its functions on colitis. In this study, we aim to investigate the protective effects of ginseng polysaccharide (WGP), its neutral fraction (WGPN) and acidic fraction (WGPA) on dextran sodium sulfate (DSS) induced colitis and the potential mechanisms with pharmacological experiments.Methods: Animal model of DSS-induced colitis was constructed by male Wistar rats. Disease activity index (DAI) scores, weight increment, colon weights, and colon length were recorded. Physiological and histological parameters, tight junctions proteins, inflammatory factors, gut microbiota, short-chain fatty acids (SCFAs) and NF-kB signalling pathway related proteins were compared among the five experimental groups, which were treated with a normal diet (Con group), DSS (DSS group), WGP (WGP group), WGPN (WGPN group), and WGPA (WGPA group), respectively. Results: Both WGP and WGPA alleviated the colitis symptoms and colon structure changes of colitis rats. They can decreased the DAIs and improved colon health; reduced colon damage and recovered intestinal barrier via regulating the tight-junction related proteins (ZO-1 and Occludin); downregulated inflammatory cytokines (IL-1β, IL-2, IL-6, and IL-17) and inhibited the TLR4/MyD88/NF-kB signalling pathway in the colon; regulated the diversity and composition of gut microbiota, especially the relative abundance of Ruminococcus; enhanced the production of SCFAs. Conclusions: WGP exerted had a protective effect against colitis through regulating NF-kB signaling pathway, recovering intestinal barrier and adjusting gut microbiota, with its acidic fraction (WGPA) primarily contributing to this activity. The results support to the utilization and investigation of ginseng polysaccharides as potential intervention strategy for the prevention of colitis.

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