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Expression data of the livers of male C57Bl6/N mice after i.p. injection of paracetamol (APAP)

ABSTRACT: Expression data of the livers of male C57Bl6/N mice after i.p. injection of paracetamol (APAP)

PROVIDER: PRJNA702769 | ENA |

REPOSITORIES: ENA

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Expression data of the livers of male C57Bl6/N mice after i.p. injection of paracetamol (APAP)

Project description:Male C57BL6/N mice were obtained from Janvier Labs (France). Mice were starved overnight before APAP administration and were fed ad libitum afterward. A single dose of 300 mg APAP/kg b.w. was intraperitoneally injected in warm phosphate-buffered saline (PBS; Table 3). The used APAP was obtained from Sigma-Aldrich (A7085-500G, Germany). The mice were sacrificed at 1, 6, and 12 hours, and on days 1, 2, 4, 6, and 8 after APAP administration. Expression data of the livers of male C57Bl6/N mice after intoxication with paracetamol (APAP)

2021-06-30 | GSE167032 | GEO

Expression data of the livers of male C57Bl6/N mice after i.p. injection of CCl4

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Expression data of the livers of male C57Bl6/N mice after i.p. injection of lipopolysaccharide (LPS)

Project description:Expression data of the livers of male C57Bl6/N mice after i.p. injection of lipopolysaccharide (LPS)

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Expression data of the livers of male C57Bl6/N mice after i.p. injection of lipopolysaccharide (LPS)

Project description:Lipopolysaccharides (LPS) are found in the outer membrane of Gram-negative bacteria. The intraperitoneal (i.p.) application of LPS into mice represents a frequently applied experimental model to induce hepatic and systemic inflammation.

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Uncovering the mechanisms responsible for intravenous paracetamol-induced hypotension

Project description:Intravenous (IV) administration of paracetamol (APAP) is well-documented to cause severe hypotension, particularly in critically ill patients. We have previously shown that a metabolite of APAP – N-acetyl-p-benzoquinone imine (NAPQI) – is a potent vasodilator, but whether APAP can be metabolised to NAPQI in the vasculature is unknown. Here, we show that NAPQI can be generated by the human coronary endothelial cells (HCAECs) treated with APAP, by staining for APAP-adducts and showing a drop in cell viability and glutathione levels, similar to direct NAPQI treatment. We show that glutathione depletion following APAP treatment is caused the cytochrome p450 enzymes (CYPs) expressed in HCAECs by utilizing a blocker of the CYPs, ketoconazole. Furthermore, mass spectrometry analysis of HCAECs treated with 10 mM APAP for 24h shows upregulation of proteins involved in redox biology and the pentose phosphate pathway, as well as CYP20A1 and POR. Lastly, we show that myeloperoxidase can also metabolize APAP to NAPQI at physiologically relevant concentrations. Taken together, this study shows that APAP can be metabolized within the vasculature to the potent vasodilator NAPQI. We suggest that this is the mechanism by which critically ill patients can present with IV APAP-induced hypotension.

2025-05-20 | PXD047218 | Pride

16S rRNA gene amplicon sequencing of gut microbiota from APAP-induced acute liver injury mice treated with Polygonatum odoratum extract

Project description:16S rRNA V3-V4 amplicon sequencing was performed on fecal samples from 12 male C57BL/6J mice across three groups (4 replicates each): Control (distilled water, 3 days), Model (distilled water, 3 days + APAP 300 mg/kg i.p.), and PoH (PO extract 3 g/kg p.o. daily for 3 days + APAP 300 mg/kg i.p.). Sequencing was performed on an Illumina NovaSeq 6000 platform using paired-end 250bp reads.

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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

Toxicoproteomics of HepG2 Reveals Translational Biomarkers of Paracetamol-Induced Liver Injury and Recovery

Project description:Drug-induced liver injury (DILI) is a leading cause of acute liver failure (ALF) and a major obstacle in drug development, reflecting the limited predictive value of animal models and lack of robust,mechanism-based biomarkers. Human in vitro systems, coupled with unbiased omics approaches, have emerged as a potential alternative strategy. Here, quantitative toxicoproteomics was applied to paracetamol (acetaminophen; APAP)-exposed HepG2 cells to identify translational biomarkers of APAP-induced DILI. Cells were exposed to the IC₅₀ concentration of APAP for 8 h (injury phase), followed by drug withdrawal and a 24 h recovery phase. LC–MS/MS analysis quantified 1,478 proteins and revealed increased protein secretion upon APAP exposure. Notably, comparison of the proteomic dataset against available enriched proteomic profiles of ALF patients’ serum confirmed the clinical relevance of the molecular signature obtained. Injury-phase upregulated proteins, including KRT18 and HMGB1, recapitulated known clinical DILI biomarkers. Conversely, recovery was characterized by enrichment of the liver regeneration markers AFP, APOA1 and HP, enabling discrimination between injury and regeneration. HPD, S100A6 and TXNRD1 emerged as candidate diagnostic biomarkers, while SERPINA1 and complement components (C3, C5) showed prognostic potential. Collectively, this study demonstrates that toxicoproteomics applied to human in vitro hepatic models, validated against patient-derived data, enables the discovery of novel translational biomarkers of liver injury and recovery.

2026-07-27 | PXD072667 | Pride

Paracetamol metabolism by endothelial cells – potential mechanism underlying intravenous paracetamol-induced hypotension

Project description:We have shown previously that a metabolite of acetaminophen (APAP), N-acetyl-p-benzoquinone imine (NAPQI), is a potent vasodilator, which could underlie the hypotension observed when APAP is administered intravenously. However, it is unknown whether APAP metabolism to NAPQI is possible in the vasculature. In this study, we examine the hypothesis that APAP is metabolized by cytochrome P450 enzymes within the endothelium, which may be accelerated in critically ill patients by the presence of elevated myeloperoxidase (MPO). Exposure of human coronary artery endothelial cells (HCAECs) to APAP resulted in the formation of protein-bound APAP adducts, together with a loss of metabolic activity. Proteomic analysis of HCAECs exposed to APAP showed upregulation of CYP20A1 and cytochrome P450 reductase (POR), together with proteins involved in the pentose phosphate pathway and maintaining redox homeostasis. Furthermore, proteomic analysis of mesenteric arteries and livers from rats administered intravenous APAP showed that APAP metabolism likely took place in the vascular wall and not in the liver. Moreover, similar proteomic pathway changes were identified in HCAECs and mesenteric arteries. Intracellular thiols were depleted in HCAECs upon APAP treatment, which was partially attenuated by ketoconazole, consistent with the involvement of cytochrome P450 enzymes (CYP) in the metabolism of APAP to a thiol-reactive metabolite such as NAPQI. Evidence was also obtained for the metabolism of APAP to a thiol-reactive intermediate by MPO, in accordance with NAPQI formation. Taken together, these data provide a putative mechanism to explain the presentation of hypotension in critically ill patients following IV APAP administration.

2025-05-20 | PXD058085 | Pride

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