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Liver tissue RNA-seq of costunolide (COS) on APAP induced liver injury

ABSTRACT: Liver tissue RNA-seq of costunolide (COS) on APAP induced liver injury

PROVIDER: PRJNA826862 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18758412_1.fastq.gz	Fastqsanger.gz
	SRR18758412_2.fastq.gz	Fastqsanger.gz
	SRR18758413_1.fastq.gz	Fastqsanger.gz
	SRR18758413_2.fastq.gz	Fastqsanger.gz
	SRR18758414_1.fastq.gz	Fastqsanger.gz

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Liver tissue RNA-seq of costunolide (COS) on APAP induced liver injury

Project description:To elucidate the potential mechanism of COS inhibiting hepatocyte death, RNA-seq technology was employed to compare the gene expression profiles of liver tissues from CON group mice, APAP group mice, and 20 mg/kg COS treatment mice.

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RNAseq on APAP, APAP+MSC, APAP+HDF at 24h

Project description:RNAseq of liver homogenate 24h after APAP (300mg/kg) exposure followed by either MSC or HDF at 90 min. MSCs, not HDFs, ameliorate APAP-induced liver injury.

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Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [mRNA_APAP]

Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.

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Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [miRNA_APAP]

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Transcriptomic profiling of differentially expressed mRNA, lncRNA, miRNA and circRNA in liver tissue of acetaminophen induced liver injury mice [circRNA_APAP]

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Oplopanax elatus Nakai chlorogenic-enriched fraction protective effect in APAP-induced liver injury

Project description:Purpose: This study investigated the protective effect and further elucidated the mechanisms of action of O. elatus on acetaminophen (APAP)-induced liver injury (AILI). Methods: O. elatus chlorogenic-enriched fraction (OEB) was administrated orally daily for seven consecutive days, followed by a single intraperitoneal injection of an overdose of APAP after the final OEB administration. Results: OEB decreased alanine aminotransferase, aspartate aminotransferase, total cholesterol, total triglycerides contents, regulated superoxide dismutase, catalase, glutathione, malondialdehyde levels, and affected the metabolism of APAP. Furthermore, OEB treatment regulated lipid metabolism, activated the peroxisome proliferator-activated receptors signaling pathway in mice with AILI, affected immune cells, and decreased neutrophil infiltration. Conclusions: This study indicated that OEB is a potential drug candidate for the prevention of APAP-induced hepatotoxicity and elucidated a potential protective mechanism by OEB.

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Effect of APAP-induced acute liver injury on WT and Nrf2KO zebrafish liver gene expression following 12 and 24 hours [RNA-Seq]

Project description:To investigate the transcriptional changes following acute liver injury, we exposed WT and Nrf2KO zebrafish larvae to APAP for 12 and 24 hours. We then dissected out zebrafish larval livers and pooled 20 livers per sample for RNA-seq.

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EV-derived miR-186-5p alleviates APAP-induced liver injury by the suppression of CXCL1

Project description:Acetaminophen (APAP) overdose is the major cause of drug-induced liver injury (DILI) and acute liver failure (ALF), and patients with advanced APAP toxicity rarely benefit from N-acetylcysteine (NAC), which is the first-line agent used in the clinic. Mesenchymal stromal cells (MSCs) and their extracellular vesicles (MSC-EVs) have shown promising effects in the treatment of DILI by decreasing neutrophil infiltration. However, the specific mechanism underlying the therapeutic effects of MSCs or MSC-EVs still needs to be elucidated. In this study, by using RNA-seq, we found that CXCL1, which is a chemoattractant for neutrophils, is a key molecule in MSC-mediated amelioration of DILI, and by luciferase reporter assay, we verified that MSC-EV-derived miR-186-5p binds to the 3’-UTR of CXCL1 to inhibit its expression in hepatocytes. Neutralizing CXCL1 reduces APAP-induced liver damage in vivo, and the agomir miR-186-5p shows excellent potential in the treatment of DILI. Overall, these findings suggest that the use of MSC-EVs may be a promising novel strategy for preventing DILI and that targeting the miR-186-5P/CXCL1 axis is a feasible approach for improving the efficacy of MSCs in the treatment of DILI.

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Project description:The well-known difference in sensitivity of mice and rats to acetaminophen (APAP) liver injury has been related to differences in the fraction that is bioactivated to the reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI). Physiologically-based pharmacokinetic modelling was used to identify doses of APAP (300 and 1000 mg/kg in mice and rats, respectively) yielding similar hepatic burdens of NAPQI, to enable the comparison of temporal liver tissue responses under conditions of equivalent chemical insult.

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RNAseq on Human APAP-ALF

Project description:Fifty percent of all acute liver failure (ALF) cases in the United States are due to acetaminophen (APAP) overdose. Assessment of canonical features of liver injury, such as plasma alanine aminotransferase activities are poor predictors of acute liver failure (ALF), suggesting the involvement of additional mechanisms independent of hepatocyte death. Previous work demonstrated a severe overdose of APAP results in impaired regeneration, the induction of senescence by p21, and increased mortality. We hypothesized that a discrete population of p21+ hepatocytes acquired a secretory phenotype that directly impedes liver recovery after a severe APAP overdose. Leveraging in-house human APAP explant liver and publicly available singlenuclei RNAseq data, we identified a subpopulation of p21+ hepatocytes enriched in a unique secretome of factors, such as Cxcl14. Spatial transcriptomics in the mouse model of APAP overdose confirmed the presence of a p21+ hepatocyte population that directly surrounded the necrotic areas. In both male and female mice, we found a dose-dependent induction of p21 and persistent circulating levels of the p21-specific constituent, Cxcl14, in the plasma after a severe APAP overdose. In parallel experiments, we targeted either the putative senescent hepatocytes with the senolytic drugs, dasatinib and quercetin, or Cxcl14 with a neutralizing antibody. We found that targeting Cxcl14 greatly enhanced liver recovery after APAP-induced liver injury, while targeting the senescent hepatocyte had no effect. This data supports that the sustained induction of p21 in hepatocytes with persistent Cxcl14 secretion are critical mechanistic events leading to ALF in mice and human patients.

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