Ontology highlight
ABSTRACT:
PROVIDER: PRJNA911510 | ENA |
REPOSITORIES: ENA
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Project description:<p><em>Parabacteroides distasonis</em> (<em>P. distasonis</em>) plays an important role in human health, including diabetes, colorectal cancer and inflammatory bowel disease. Here, we show that <em>P. distasonis</em> is decreased in patients with hepatic fibrosis, and that administration of P. distasonis to mice improves thioacetamide (TAA)- and methionine and choline deficient (MCD) diet-induced hepatic fibrosis. <em>P. distasonis</em> was associated with increased bile salt hydrolase (BSH) activity and inhibition of intestinal farnesoid X receptor (FXR) signaling leading to decreased taurochenodeoxycholic acid (TCDCA) levels in liver. The decrease of TCDCA improved activation of hepatic stellate cells (HSCs) through decreasing the mitochondrial permeability transition (MPT)-Caspase-11 pyroptosis pathway. Celastrol was demonstrated as a promoter of <em>P. distasonis</em>, which could inhibit intestinal FXR and increase the excretion of bile acids, leading to decreased hepatic TCDCA and prevention against TAA- and MCD diet-induced hepatic fibrosis. These data suggest that supplementation of <em>P. distasonis</em> may be a promising means to ameliorate hepatic fibrosis.</p><p><br></p><p><strong>Hepatic fibrosis serum+feces (sample 3) analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS6728' rel='noopener noreferrer' target='_blank'><strong>MTBLS6728</strong></a>.</p><p><strong>Hepatic fibrosis serum (sample 1) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6732' rel='noopener noreferrer' target='_blank'><strong>MTBLS6732</strong></a>.</p><p><strong>Hepatic fibrosis feces (sample 2) analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS6742' rel='noopener noreferrer' target='_blank'><strong>MTBLS6742</strong></a>.</p>
2023-03-17 | MTBLS6728 | MetaboLights
Project description:The aim is to characterize rat liver fibrosis induced by thioacetamide (TAA). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) were treated with thioacetamide (TAA). Rat liver samples were collected from five groups of rats at week 1, 2, 4, 8 and 13 after TAA (300 mg/kg) administration three times per week while five control groups receive the same volume of 0.9% normal saline. Four biological replicates were used for each group.
2021-09-29 | E-MTAB-10547 | biostudies-arrayexpress
Project description:Ginkgetin could significantly attenuate liver fibrosis in a rat model induced by TAA, including inhibiting hepatic inflammtion and fibrosis. In addition, the related signaling pathways and gene expression were also downregulated by ginkgetin by bulk RNA Sequencing analysis.
2023-09-01 | GSE242212 | GEO
Project description:Ginkgetin could significantly attenuate liver fibrosis in a mouse model induced by TAA, including inhibiting hepatic inflammtion and fibrosis. In addition, the related signaling pathways and gene expression were also downregulated by ginkgetin by bulk RNA Sequencing analysis.
2023-08-03 | GSE236779 | GEO
Project description:Metabolomic analysis on hepatic stellate cells isolated from PBS- or thioacetamide (TAA)-treated wild-type and Cyp1b1 knockout mice was performed to determine the metabolic basis by which CYP1B1 ablation inhibits HSC activation and liver fibrosis.
2024-08-28 | MSV000095716 | MassIVE
Project description:Purpose: The goals of this study was to (1) evaluate the protective effect of celastrol on alpha-naphthylisothiocyanate (ANIT)-induced cholestasis and (2) which genes were recovered by celastrol. Methods:To investigate the protective effect of celastrol on ANIT-induced cholestasis, the WT mice were randomly assigned into two groups, respectively (n=3): (1) ANIT; (2) ANIT+Celastrol. ANIT+Celastrol group was orally treated with celastrol (10 mg/kg dissolved in 1% DMSO + 2% Tween 80 + 97% water) for 5 consecutive days. After celastrol was treated for 3 days, ANIT and ANIT+Celastrol groups were given a single oral dose of ANIT. All mice were killed 48 h after ANIT administration. Liver samples were harvested and frozen at -80 °C before analysis. Results: A total of 978 DEGs were identified. Large numbers of these DEGs were related to activation of SIRT1, which included increased FXR signaling and inhibition of PPARγ, nuclear factor-kappa B (NF-κB), and P53 signaling. Conclusions: Celastrol could protect ANIT-induced cholestasis by recovering disrupted Sirt1 level.
2018-02-09 | GSE110391 | GEO
Project description:Objectives: Scleroderma (systemic sclerosis, SSc), as a prototypic inflammation-driven fibrotic disease, possesses connective tissue lesions populated with persistently activated myofibroblasts maintained by an mechanotranductive/pro-adhesive signaling loop. Drugs targeting this pathway are therefore of likely therapeutic benefit. The mechanosensitive transcriptional co-activator, yes activated protein-1 (YAP1), is activated in SSc fibroblasts. The terpenoid celastrol has recently been identified as a YAP1 inhibitor: however, if celastrol can alleviate SSc fibrosis is unknown. Methods: Human dermal fibroblasts from healthy individuals and patients with diffuse cutaneous SSc were treated with or without transforming growth factor b1 (TGFb1) in the presence or absence of celastrol. C57BL6J mice were subjected to the inflammatory-driven bleomycin-induced model of skin SSc, in the presence or absence of celastrol. RNA expression was assessed using RNAseq, real-time polymerase chain reaction and spatial transcriptomic analyses. Protein expression was determined using Western blot and enzyme-linked immunosorbent assay. Fibrosis was monitored by hematoxylin and eosin and trichrome staining, and indirect immunofluorescence analysis. Results: In dermal fibroblasts, celastrol impaired the ability of TGFβ1 to induce an SSc-like pattern of gene expression, including the induction of cellular communication network factor 2 (CCN2), collagen I and TGFβ1 protein. Celastrol alleviated the persistent fibrotic phenotype of dermal fibroblasts cultured from lesions of SSc patients. In the bleomycin-induced model of SSc dermatopathology, celastrol inhibited fibrosis and blocked nuclear localization of YAP in myofibroblasts. Conclusion: Our data are consistent with the hypothesis that compounds, such as celastrol, that antagonize the YAP pathway may be potential treatments for SSc skin fibrosis.
2023-11-01 | GSE226760 | GEO
Project description:Objectives: Scleroderma (systemic sclerosis, SSc), as a prototypic inflammation-driven fibrotic disease, possesses connective tissue lesions populated with persistently activated myofibroblasts maintained by an mechanotranductive/pro-adhesive signaling loop. Drugs targeting this pathway are therefore of likely therapeutic benefit. The mechanosensitive transcriptional co-activator, yes activated protein-1 (YAP1), is activated in SSc fibroblasts. The terpenoid celastrol has recently been identified as a YAP1 inhibitor: however, if celastrol can alleviate SSc fibrosis is unknown. Methods: Human dermal fibroblasts from healthy individuals and patients with diffuse cutaneous SSc were treated with or without transforming growth factor b1 (TGFb1) in the presence or absence of celastrol. C57BL6J mice were subjected to the inflammatory-driven bleomycin-induced model of skin SSc, in the presence or absence of celastrol. RNA expression was assessed using RNAseq, real-time polymerase chain reaction and spatial transcriptomic analyses. Protein expression was determined using Western blot and enzyme-linked immunosorbent assay. Fibrosis was monitored by hematoxylin and eosin and trichrome staining, and indirect immunofluorescence analysis. Results: In dermal fibroblasts, celastrol impaired the ability of TGFβ1 to induce an SSc-like pattern of gene expression, including the induction of cellular communication network factor 2 (CCN2), collagen I and TGFβ1 protein. Celastrol alleviated the persistent fibrotic phenotype of dermal fibroblasts cultured from lesions of SSc patients. In the bleomycin-induced model of SSc dermatopathology, celastrol inhibited fibrosis and blocked nuclear localization of YAP in myofibroblasts. Conclusion: Our data are consistent with the hypothesis that compounds, such as celastrol, that antagonize the YAP pathway may be potential treatments for SSc skin fibrosis.
2023-11-01 | GSE226375 | GEO
Project description:Objectives: Scleroderma (systemic sclerosis, SSc), as a prototypic inflammation-driven fibrotic disease, possesses connective tissue lesions populated with persistently activated myofibroblasts maintained by an mechanotranductive/pro-adhesive signaling loop. Drugs targeting this pathway are therefore of likely therapeutic benefit. The mechanosensitive transcriptional co-activator, yes activated protein-1 (YAP1), is activated in SSc fibroblasts. The terpenoid celastrol has recently been identified as a YAP1 inhibitor: however, if celastrol can alleviate SSc fibrosis is unknown. Methods: Human dermal fibroblasts from healthy individuals and patients with diffuse cutaneous SSc were treated with or without transforming growth factor b1 (TGFb1) in the presence or absence of celastrol. C57BL6J mice were subjected to the inflammatory-driven bleomycin-induced model of skin SSc, in the presence or absence of celastrol. RNA expression was assessed using RNAseq, real-time polymerase chain reaction and spatial transcriptomic analyses. Protein expression was determined using Western blot and enzyme-linked immunosorbent assay. Fibrosis was monitored by hematoxylin and eosin and trichrome staining, and indirect immunofluorescence analysis. Results: In dermal fibroblasts, celastrol impaired the ability of TGFβ1 to induce an SSc-like pattern of gene expression, including the induction of cellular communication network factor 2 (CCN2), collagen I and TGFβ1 protein. Celastrol alleviated the persistent fibrotic phenotype of dermal fibroblasts cultured from lesions of SSc patients. In the bleomycin-induced model of SSc dermatopathology, celastrol inhibited fibrosis and blocked nuclear localization of YAP in myofibroblasts. Conclusion: Our data are consistent with the hypothesis that compounds, such as celastrol, that antagonize the YAP pathway may be potential treatments for SSc skin fibrosis.
2023-11-01 | GSE226374 | GEO
Project description:Purpose: The goal of this study is to investigate the effect of recombinant human Cytoglobin (rhCYGB) on liver fibrosis induced by TAA in mice. Method: mRNA profiles of liver tissues from TAA-control mice and TAA-rhCYGB treated mice were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes and fibrosis-related genes were down-regulated by the rhCYGB treatment.
2020-08-25 | GSE156777 | GEO