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Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [16S]

ABSTRACT: Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [16S]

PROVIDER: PRJNA893614 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22033623_1.fastq.gz	Fastqsanger.gz
	SRR22033623_2.fastq.gz	Fastqsanger.gz
	SRR22033624_1.fastq.gz	Fastqsanger.gz
	SRR22033624_2.fastq.gz	Fastqsanger.gz
	SRR22033625_1.fastq.gz	Fastqsanger.gz

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Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [16S]

Project description:Ulcerative colitis (UC) is a complex immune-mediated inflammatory disease. In recent years, the incidence of UC has increased rapidly, however, its exact etiology and mechanism are still unclear. Based on the definite anti-inflammatory and antibacterial activities of Sanguisorba officinalis L., we studied its monomer methyl gallate (MG). In this study, we employed flow cytometry and detected nitric oxide production, finding MG regulated macrophage polarization and inhibited the expression of proinflammatory cytokines in vitro. MG also exhibited anti-inflammatory activity with ameliorating body weight loss, improving colon length and histological damage in dextran sulfate sodium-induced UC mice. Meanwhile, transcription sequencing and 16S rRNA sequencing analyzed the key signaling pathways and changes in the gut microbiota of MG for UC treatment, proving MG could alleviate inflammation by regulating the TLR4/NF-κB pathway in vivo and in vitro. Additionally, MG altered the diversity and composition of the gut microbiota and changed the abundance of metabolic products. In conclusion, our results are the first to demonstrate MG has obvious therapeutic effects against acute UC, which is related to macrophage polarization, improved intestinal flora dysbiosis and inhibition of TLR4/NF-κB signaling pathway activation, and may be a promising therapeutic agent for UC treatment.

2024-05-31 | GSE216433 | GEO

Methyl Gallate Alleviates Acute Ulcerative Colitis by Modu-lating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [RNA-seq]

2024-05-31 | GSE216434 | GEO

Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway

Project description:Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway

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Methyl Gallate Alleviates Acute Ulcerative Colitis by Modu-lating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [RNA-seq]

Project description:Methyl Gallate Alleviates Acute Ulcerative Colitis by Modu-lating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway [RNA-seq]

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Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-31 | GSE216435 | GEO

TLR4/NF-κB-responsive microRNAs in a mouse model of skeletal muscle ischemia-reperfusion injury

Project description:TLR4/NF-κB signaling plays a central mediator in response to danger signals released in the muscle ischemia-reperfusion injury (IRI). This study was designed to profile TLR4/NF-κB-responsive microRNAs (miRNAs) in the skeletal muscles following IRI. Following 2 h of ischemia and subsequent reperfusion for indicated times (0 h, 4 h, 1 d, and 7 d) of the isolated thigh skeletal muscles based on femoral artery perfusion of C57BL/6, Tlr4–/–, and NF-κB–/–mice, the muscle specimens were analyzed with an miRNA array to detect the TLR4/NF-κB-responsive miRNAs.

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iTRAQ analysis of ClpP mutant treated with methyl gallate

Project description:Methyl gallate (MG) is an effective microbicide with great potential usefulness in the integrated management of plant diseases and an important potential drug for clinical application. However, its target remains unknown. This study conducted a transposon sequencing (Tn-seq) under MG treatment in plant pathogenic bacterium Ralstonia solanacearum. Tn-seq identified that the mutation of caseinolytic protease proteolytic subunit gene clpP significantly increased the resistance of R. solanacearum to MG, which was validated by the in-frame gene deletion. iTRAQ proteomics analysis was then employed and revealed that chemotaxis and flagella associated proteins were the major substrates degraded by ClpP under the tested condition. Moreover, sulfur metabolism associated proteins were also possible substrates of ClpP and were up-regulated by MG treatment in the wild type R. solanacearum but not in the clpP mutant. Furthermore, molecular docking confirmed the possible interaction between MG and ClpP. Taken together, this study revealed that MG may target bacterial ClpP, inhibit the activity of ClpP, and consequently disorder bacterial proteostasis, providing a theoretical basis for the application of MG.

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2019-03-27 | MODEL1809230001 | BioModels

Echinatin alleviates inflammation and pyroptosis in hypoxic-ischemic brain damage by inhibiting TLR4/ NF-κB pathway

Project description:Echinatin alleviates inflammation and pyroptosis in hypoxic-ischemic brain damage by inhibiting TLR4/ NF-κB pathway

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Disulfiram blocks inflammatory TLR4 signaling by targeting MD-2

Project description:Toll-like receptor 4 (TLR4) sensing of lipopolysaccharide (LPS), the most potent pathogen-associated molecular pattern of gram-negative bacteria, activates NF-κB and Irf3, which induces inflammatory cytokines and interferons that trigger an intense inflammatory response, which is critical for host defense but can also cause serious inflammatory pathology, including sepsis. Although TLR4 inhibition is an attractive therapeutic approach for suppressing overexuberant inflammatory signaling, previously identified TLR4 antagonists have not shown any clinical benefit. Here, we identify disulfiram (DSF), an FDA-approved drug for alcoholism, as a specific inhibitor of TLR4-mediated inflammatory signaling. TLR4 cell surface expression, LPS sensing, dimerization and signaling depend on TLR4 binding to MD-2. DSF and other cysteine-reactive drugs, previously shown to block LPS-triggered inflammatory cell death (pyroptosis), inhibit TLR4 signaling by covalently modifying Cys133 of MD-2, a key conserved residue that mediates TLR4 sensing and signaling. DSF blocks LPS-triggered inflammatory cytokine, chemokine, and interferon production by macrophages in vitro. In the aggressive N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson’s disease (PD) in which TLR4 plays an important role, DSF markedly suppresses neuroinflammation and dopaminergic neuron loss, and restores motor function. Our findings identify a role for DSF in curbing TLR4-mediated inflammation and suggest that DSF and other drugs that target MD-2 might be useful for treating PD and other diseases in which inflammation contributes importantly to pathogenesis.

2023-08-07 | GSE237028 | GEO

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