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Ginsenoside Rd monomer alleviates ulcerative colitis by regulating miRNAs and target genes in macrophages

ABSTRACT: Ginsenoside Rd monomer alleviates ulcerative colitis by regulating miRNAs and target genes in macrophages

PROVIDER: PRJNA970369 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24471268.fastq.gz	Fastqsanger.gz
	SRR24471269.fastq.gz	Fastqsanger.gz
	SRR24471270.fastq.gz	Fastqsanger.gz
	SRR24471271.fastq.gz	Fastqsanger.gz
	SRR24471272.fastq.gz	Fastqsanger.gz

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Ginsenoside Rd monomer alleviates ulcerative colitis by regulating miRNAs and target genes in macrophages

Project description:to discover the miRNAs involved in the production of cytokines by RAW264.7 cells treated with LPS and ginsinoside Rd monomer We then performed gene expression profiling analysis using data obtained from RNA-seq of RAW264.7 cells.

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Gene expression data from DMD patient hiPSC-derived myoblasts treated with fenofibrate, ginsenoside Rd or DMSO

Project description:Drug development costs a significant amount of time and resources for new pharmaceutical drugs. However, the progress has been limited for orphan diseases such as Duchenne muscular dystrophy (DMD). By using human induced pluripotent stem cells (hiPSCs), here we show an exemplary drug screening campaign and the identification of two potential drugs effective in a DMD mouse model. We developed a DMD-hiPSC screening platform utilizing high-content imaging to identify hit compounds that enhance myogenic fusion abilities of patient-specific myoblasts. Among 1524 compounds (Johns Hopkins Clinical Compound library), two hit compounds restored in vitro fusion defects of DMD patient hiPSC-derived myoblasts. Transcriptional profiling revealed that the function of two hit compounds, ginsenoside Rd (natural product, ginseng extract) and fenofibrate (FDA-approved drug), are associated with FLT3 signaling and TGF-β signaling, respectively. The preclinical tests in mdx mice show that the treatment of the two hit compounds can ameliorate the skeletal muscle and behavioral phenotypes caused by DYSTROPHIN deficiency, suggesting therapeutic potential of these two compounds. Our study demonstrates the feasibility of early-stage drug development for rare diseases using symptom-relevant cells derived from patient-specific hiPSCs.

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Haemophilus influenzae Rd KW20 strain:Rd

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Gene expression data from DMD patient hiPSC-derived myoblasts treated with fenofibrate, ginsenoside Rd or DMSO

Project description:Gene expression data from DMD patient hiPSC-derived myoblasts treated with fenofibrate, ginsenoside Rd or DMSO

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lncRNA sequencing of human ovarian cancer cell SKOV3 after exposure to ginsenoside 20(S)-Rg3

Project description:Ginsenoside 20(S)-Rg3, an active saponin monomer extracted from red ginseng, inhibits the malignancy of ovarian cancer cells. RNA-Seq analysis was used for deep sequencing of lncRNA to detected molecular mechanisms of 20(S)-Rg3.We identified 85 differentially expressed lncRNA influenced by 20(S)-Rg3, among which 67 lncRNAs were significantly decreased (fold change<0.5, p<0.05) including 12 ncRNAs and 55 pseudo genes, and 18 lncRNAs were significantly increased (fold change>1.5, p<0.05) including 3 ncRNAs, 14 pseudo genes and 1 unknown gene. This study provide a valuable resource for the discovery of lncRNAs related to anti-tumor mechanism of 20(S)-Rg3.

2021-02-16 | GSE118216 | GEO

Outer membrane vesicle and outer membrane of Haemophilus influenzae Rd KW20, Rd ∆yrbE and Rd ∆vacJ

Project description:Bacterial outer membrane vesicles (OMVs) have important biological roles in pathogenesis and intercellular interactions, but a general mechanism of OMV formation is lacking. Here we show that the VacJ/Yrb ABC transport system, a proposed phospholipid (PL) transporter, is involved in OMV formation. Deletion or repression of VacJ/Yrb increases OMV production in two distantly related Gram-negative bacteria, Haemophilus influenzae and Vibrio cholerae. Within our studies we also analyzed the proteome of the OMV and outer membrane (OM) and found no massive alteration in Haemophilus influenzae Rd KW20, Rd ∆yrbE and Rd ∆vacJ. Lipidome analyses demonstrate that OMVs from VacJ/Yrb-defective mutants in H. influenzae are enriched in PLs and certain fatty acids. Furthermore, we demonstrate that OMV production and regulation of the VacJ/Yrb ABC transport system respond to iron starvation. Our results suggest a new general mechanism of OMV biogenesis based on PL accumulation in the outer leaflet of the outer membrane. This mechanism is highly conserved among Gram-negative bacteria, provides a means for regulation, can account for OMV formation under all growth conditions, and might have important pathophysiological roles in vivo.

2016-01-27 | PXD003249 | Pride

RD effect on PC-3 cells

Project description:RD induced DNA damage and suppressed DNA repair in PC-3 cells. Expression profiling of PC-3 cells treated with 10 umol/L RD for 24 hours.

2012-05-08 | GSE37812 | GEO

RD effect on PC-3 cells

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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.

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