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

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

PROVIDER: PRJNA756103 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15522100_1.fastq.gz	Fastqsanger.gz
	SRR15522100_2.fastq.gz	Fastqsanger.gz
	SRR15522101_1.fastq.gz	Fastqsanger.gz
	SRR15522101_2.fastq.gz	Fastqsanger.gz
	SRR15522096_1.fastq.gz	Fastqsanger.gz

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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.

2021-08-20 | GSE182399 | GEO

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

Project description:RNAseq on APAP, APAP+MSC, APAP+HDF at 24h

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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.

2022-09-16 | GSE198277 | GEO

Hepatic responses of mice and rats to equivalent acetaminophen (APAP) insult [rat]

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.

2023-06-20 | GSE205202 | GEO

Hepatic responses of mice and rats to equivalent acetaminophen (APAP) insult [mouse]

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Protein profiles of ACUTE liver injury in mice mediated by CCl4 or APAP

Project description:Mice were treated with CCl4,APAP or olive oil for 24 h, protein changes were detected by mass spectrometry

2024-10-05 | PXD029204 | Pride

Identification of Novel Regulatory Genes in APAP Induced Hepatocyte Toxicity by a Genome-Wide CRISPR-Cas9 Screen

Project description:Acetaminophen (APAP) is a commonly used analgesic responsible for more than half of acute liver failure cases. Identification of previously unknown genetic risk factors would provide mechanistic insights and novel therapeutic targets for APAP-induced liver injury. This study used a genome-wide CRISPR-Cas9 screen to evaluate genes that are protective against, or cause susceptibility to, APAP-induced liver injury. HuH7 human hepatocellular carcinoma cells containing CRISPR-Cas9 gene knockouts were treated with 15mM APAP for 30 minutes to 4 days. A gene expression profile was developed based on the 1) top screening hits, 2) overlap of expression data from APAP overdose studies, and 3) predicted affected biological pathways. We further demonstrated the implementation of intermediate time points for the identification of early and late response genes. This study illustrated the power of a genome-wide CRISPR-Cas9 screen to systematically identify novel genes involved in APAP-induced hepatotoxicity and to provide potential targets to develop novel therapeutic modalities.

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Hepatic responses of mice and rats to equivalent acetaminophen (APAP) insult – SWATH proteomics

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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.

2024-04-15 | GSE255777 | GEO

RNAseq on APAP mice flow sorted macrophages at 72h

Project description:RNAseq of flow sorted macrophages 72h after APAP. Cxcr4 expression induced on subpopulation of macrophages after APAP.

2022-05-31 | GSE199249 | GEO