Dimethyl fumarate ameliorates dextran sulfate sodium-induced murine experimental colitis by activating Nrf2 and suppressing NLRP3 inflammasome activation

Liu, Xiuting; Zhou, Wei; Zhang, Xin; Lü, Ping; Du, Qianming; Tao, Lei; Ding, Yang; Wang, Yajing; Hu, Rong

doi:10.1016/j.bcp.2016.05.002

Cited by 135 publications

(100 citation statements)

References 41 publications

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“…In agreement with the in vivo data, pretreatment of inflammasome-activated human monocytic THP-1 cells with DMF decreased mRNA levels of NLRP3 and pro-IL-1 [30] .…”

Section: Nlrp3 Priming By Metabolitessupporting

confidence: 77%

“…Interestingly, DMF has been reported to be beneficial in the treatment of a mouse model of dextran sulfate sodium (DSS)-induced colitis by decreasing NLRP3 expression and activation in an Nrf2-dependent manner [30] . In agreement with the in vivo data, pretreatment of inflammasome-activated human monocytic THP-1 cells with DMF decreased mRNA levels of NLRP3 and pro-IL-1 [30] .…”

Section: Nlrp3 Priming By Metabolitesmentioning

confidence: 99%

See 1 more Smart Citation

Inflammasome Priming in Sterile Inflammatory Disease

Patel

Carroll

Galván-Peña

et al. 2017

Trends in Molecular Medicine

211

167

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“…In agreement with the in vivo data, pretreatment of inflammasome-activated human monocytic THP-1 cells with DMF decreased mRNA levels of NLRP3 and pro-IL-1 [30] .…”

Section: Nlrp3 Priming By Metabolitessupporting

confidence: 77%

Section: Nlrp3 Priming By Metabolitesmentioning

confidence: 99%

Inflammasome Priming in Sterile Inflammatory Disease

Patel

Carroll

Galván-Peña

et al. 2017

Trends in Molecular Medicine

211

167

View full text Add to dashboard Cite

“…Consistent with the above data, two recent papers by Wang et al (58) and Liu et al (62) have reported that the inhibition of ROS formation exerted beneficial effects in colitis through the blockade of NLRP3 assembly (58, 62). In particular, these authors observed that two small molecules, 3-(2-oxo-2-phenylethylidene)-2,3,6,7-tetrahydro-1H-pyrazino-[2,1-a]isoquinolin-4(11bH)-one (compound 1) and dimethyl fumarate, promote the transcription of genes coding for various detoxification and antioxidant enzymes, through the activation of NFE-related factor 2 (Nrf2).…”

Section: Pharmacological Modulation Of Nlrp3 Inflammasome In Bowel Insupporting

confidence: 70%

Canonical and Non-Canonical Activation of NLRP3 Inflammasome at the Crossroad between Immune Tolerance and Intestinal Inflammation

et al. 2017

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Several lines of evidence point out the relevance of nucleotide-binding oligomerization domain leucine rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome as a pivotal player in regulating the integrity of intestinal homeostasis and shaping innate immune responses during bowel inflammation. Intensive research efforts are being made to achieve an integrated view about the protective/detrimental role of canonical and non-canonical NLRP3 inflammasome activation in the maintenance of intestinal microenvironment integrity. Evidence is also emerging that the pharmacological modulation of NLRP3 inflammasome could represent a promising molecular target for the therapeutic management of inflammatory immune-mediated gut diseases. The present review has been intended to provide a critical appraisal of the available knowledge about the role of canonical and non-canonical NLRP3 inflammasome activation in the dynamic interplay between microbiota, intestinal epithelium, and innate immune system, taken together as a whole integrated network regulating the maintenance/breakdown of intestinal homeostasis. Moreover, special attention has been paid to the pharmacological modulation of NLRP3 inflammasome, emphasizing the concept that this multiprotein complex could represent a suitable target for the management of inflammatory bowel diseases.

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“…The colonic levels of various caspases were shown to be increased post colitis induction. For example, the levels of caspase-3 [81, 82, 86], -7 [81] and -12 [76], and the cleaved form of caspases-1 [87, 88], -12, and -7 [73] were increased in the colonic tissues in various animal models of colitis, which are also in agreement with our findings in regard to caspase-3 and -8 levels (Fig 5). …”

Section: Discussionsupporting

confidence: 91%

Anti-Inflammatory Properties of the Enaminone E121 in the Dextran Sulfate Sodium (DSS) Colitis Model

2016

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BackgroundEnaminones are synthetic compounds with an established role in the prevention of various forms of seizures. Recent evidence suggests potent anti-tussive, bronchodilation and anti-inflammatory properties. Pre-treatment with particularly E121 compound resulted in a decrease in leukocyte recruitment in the ovalbumin induced-model of asthma, immune cell proliferation and cytokine release in vitro. We hypothesize that E121 might serve as a therapeutic potential in intestinal inflammation through modulating immune cell functions.MethodsColitis was induced by daily dextran sulfate sodium (DSS) administration for 5 days, and its severity was determined by gross and histological assessments. The plasma level of various cytokines was measured using flow cytometry-based assay. The colonic expression/ phosphorylation level of various molecules was determined by immunofluorescence and western blotting. The effects of E121 treatment on in vitro neutrophil chemotaxis (under-agarose assay), superoxide release (luminol oxidation assay) and apoptosis (annexin V/7AAD) were also determined.ResultsDSS-induced colitis in mice was significantly reduced by daily E121 treatment (30–100 mg/kg) at gross and histological levels. This effect was due to modulated plasma levels of interleukin (IL-2) and colonic expression levels of various signaling molecules and proteins involved in apoptosis. In vitro neutrophil survival, chemotaxis, and superoxide release were also reduced by E121 treatment.ConclusionOur results indicate important anti-inflammatory actions of E121 in the pathogenesis of IBD.

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Dimethyl fumarate ameliorates dextran sulfate sodium-induced murine experimental colitis by activating Nrf2 and suppressing NLRP3 inflammasome activation

Cited by 135 publications

References 41 publications

Inflammasome Priming in Sterile Inflammatory Disease

Inflammasome Priming in Sterile Inflammatory Disease

Canonical and Non-Canonical Activation of NLRP3 Inflammasome at the Crossroad between Immune Tolerance and Intestinal Inflammation

Anti-Inflammatory Properties of the Enaminone E121 in the Dextran Sulfate Sodium (DSS) Colitis Model

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