Gadolinium chloride improves the course of TNBS and DSS-induced colitis through protecting against colonic mucosal inflammation

Du, Chao; Wang, Peng; Yu, Yanbo; Chen, Feixue; Liu, Jun; Li, Yanqing

doi:10.1038/srep06096

Cited by 27 publications

(25 citation statements)

References 27 publications

(39 reference statements)

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“…The perpetuated activation of NF-κB in patients with active IBD suggests that regulation of NF-κB activity is a very attractive target for therapeutic intervention. Many chemicals, such as gadolinium chloride and porcine β-defensin 2 could ameliorate UC through inhibition of the NF-κB signaling pathway [17, 23]. Consistent with a previous study [24], CaA could suppress the pro-inflammatory response by blocking the activation of NF-κB.…”

Section: Discussionsupporting

confidence: 72%

Caffeic acid ameliorates colitis in association with increasedAkkermansiapopulation in the gut microbiota of mice

et al. 2016

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Emerging evidence shows that dietary agents and phytochemicals contribute to the prevention and treatment of ulcerative colitis (UC). We first reported the effects of dietary caffeic acid (CaA) on murine experimental colitis and on fecal microbiota. Colitis was induced in C57BL/6 mice by administration of 2.5% dextran sulfate sodium (DSS). Mice were fed a control diet or diet with CaA (1 mM). Our results showed that dietary CaA exerted anti-inflammatory effects in DSS colitis mice. Moreover, CaA could significantly suppress the secretion of IL-6, TNFα, and IFNγ and the colonic infiltration of CD3+ T cells, CD177+ neutrophils and F4/80+ macrophages via inhibition of the activation of NF-κB signaling pathway. Analysis of fecal microbiota showed that CaA could restore the reduction of richness and inhibit the increase of the ratio of Firmicute to Bacteroidetes in DSS colitis mice. And CaA could dramatically increase the proportion of the mucin-degrading bacterium Akkermansia in DSS colitis mice. Thus, CaA could ameliorate colonic pathology and inflammation in DSS colitis mice, and it might be associated with a proportional increase in Akkermansia.

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Section: Discussionsupporting

confidence: 72%

Caffeic acid ameliorates colitis in association with increasedAkkermansiapopulation in the gut microbiota of mice

et al. 2016

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“…It seems that clodronate depletes M2 macrophages in the colon (79), yet it is unclear whether gadolinium chloride depletes colonic M1 macrophages. It has recently been shown that treatment with gadolinium chloride ameliorates colitis in mice treated with TNBS or DSS (19). This study did not find a significant reduction in macrophages in the colon of mice treated with gadolinium chloride, but this could be attributed to the use of F4/80 as the macrophage marker, as proinflammatory macrophages in the colon express low levels of F4/80 (7,96).…”

Section: Colonic Macrophages As Therapeutic Targets and Probiotic Thecontrasting

confidence: 64%

Colonic macrophage polarization in homeostasis, inflammation, and cancer

Isidro

Appleyard

2016

American Journal of Physiology-Gastrointestinal and Liver Physi

177

153

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Our review focuses on the colonic macrophage, a monocyte-derived, tissue-resident macrophage, and the role it plays in health and disease, specifically in inflammatory conditions such as inflammatory bowel disease and cancer of the colon and rectum. We give special emphasis to macrophage polarization, or phenotype, in these different states. We focus on macrophages because they are one of the most numerous leukocytes in the colon, and because they normally contribute to homeostasis through an anti-inflammatory phenotype. However, in conditions such as inflammatory bowel disease, proinflammatory macrophages are increased in the colon and have been linked to disease severity and progression. In colorectal cancer, tumor cells may employ anti-inflammatory macrophages to promote tumor growth and dissemination, whereas proinflammatory macrophages may antagonize tumor growth. Given the key roles that this cell type plays in homeostasis, inflammation, and cancer, the colonic macrophage is an intriguing therapeutic target. As such, potential macrophage-targeting strategies are discussed.

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“…Out of them, ulcerative colitis is the major form of IBD and mainly affecting the colonic mucosa and submucosa. 6 In addition, the upregulation of certain proteins, i.e., cyclooxygenase (COX)-2 or inducible nitric oxide synthase (iNOS) supporting a critical role in the pathogenesis of ulcerative colitis. 5 The etiology of ulcerative colitis is complex and remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Oral administration of geraniol ameliorates acute experimental murine colitis by inhibiting pro-inflammatory cytokines and NF-κB signaling

et al. 2015

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Ulcerative colitis is associated with a considerable reduction in the quality of life of patients. The use of phyto-ingredients is becoming an increasingly attractive approach for the management of colitis. Geraniol is a monoterpene with anti-inflammatory and antioxidative properties. In this study, we investigated the therapeutic potential of geraniol as a complementary and alternative medicine against dextran sulphate sodium (DSS)-induced ulcerative colitis in mice. Disease activity indices (DAI) comprising body weight loss, presence of occult blood and stool consistency were assessed for evaluation of colitis symptoms. Intestinal damage was assessed by evaluating colon length and its histology. Pre-treatment with geraniol significantly reduced the DAI score, improved stool consistency (without occult blood) and increased the colon length. The amount of pro-inflammatory cytokines, specifically TNF-α, IL-1β and IL-6 and the activity of myeloperoxidase in colon tissue were significantly decreased in geraniol pre-treated mice. Western blot analyses revealed that geraniol interfered with NF-κB signaling by inhibiting NF-κB (p65)-DNA binding, and IκBα phosphorylation, degradation and subsequent increase in nuclear translocation. Moreover, the expressions of downstream target pro-inflammatory enzymes such as iNOS and COX-2 were significantly reduced by geraniol. Pre-treatment with geraniol also restored the DSS-induced decline in antioxidant parameters such as reduced glutathione and superoxide dismutase activity and attenuated the increase in lipid peroxidation marker, thiobarbituric acid reactive substances and nitrative stress marker, nitrites in colon tissue. Thus, our results suggest that geraniol is a potential therapeutic agent for inflammatory bowel disease.

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Gadolinium chloride improves the course of TNBS and DSS-induced colitis through protecting against colonic mucosal inflammation

Cited by 27 publications

References 27 publications

Caffeic acid ameliorates colitis in association with increasedAkkermansiapopulation in the gut microbiota of mice

Caffeic acid ameliorates colitis in association with increasedAkkermansiapopulation in the gut microbiota of mice

Colonic macrophage polarization in homeostasis, inflammation, and cancer

Oral administration of geraniol ameliorates acute experimental murine colitis by inhibiting pro-inflammatory cytokines and NF-κB signaling

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