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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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Project description:The series was designed to identify the different methylated single CpGs involved in the pathophysiology of ulcerative colitis. A cohort of n=20 monozygotic twins, discordant for ulcerative colitis was selected. Illumina and Nimblegen platforms were used.

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Ginsenoside Rg1 Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Microbial Tryptophan Metabolism.

Project description:Ulcerative colitis (UC) is a chronic and recurrent inflammatory disorder in the gastrointestinal tract. Here, we examined the pharmacological effects of ginsenoside Rg1, a natural compound with low bioavailability, on the acute experimental colitis mice induced by dextran sulfate sodium (DSS) and explored underlying mechanisms. Acute UC was induced in C57BL/6 mice by 2.5% DSS for 7 days, meanwhile, 2 mg/10 g b.w. ginsenoside Rg1 was administrated to treat the mice. Body weight, colon length, colon tissue pathology, and colon tissue inflammatory cytokines were assessed. The composition structure of gut microbiota was profiled using 16s rRNA sequencing. Global metabolomic profiling of the feces was performed, and tryptophan and its metabolites in the serum were detected. The results showed that Rg1 significantly ameliorated DSS-induced colonic injury and colonic inflammation. In addition, Rg1 also partly reversed the imbalance of gut microbiota composition caused by DSS. Rg1 intervention can regulate various metabolic pathways of gut microbiota such as valine, leucine, and isoleucine biosynthesis and vitamin B6 metabolism and the most prominent metabolic alteration was tryptophan metabolism. DSS decreased the levels of tryptophan metabolites in the serum, including indole-3-carboxaldehyde, indole-3-lactic acid, 3-indolepropionic acid, and niacinamide and Rg1 can increase the levels of these metabolites. In conclusion, the study discovered that Rg1 can protect the intestinal barrier and alleviate colon inflammation in UC mice, and the underlying mechanism is closely related to the regulation of gut microbiota composition and microbial tryptophan metabolism.

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