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Project description:Acetaminophen (APAP) overdose can cause acute kidney injury (AKI), but its molecular mechanisms remain poorly understood and no effective treatments are currently available. In this study, we performed an integrated analysis combining transcriptomic, proteomic, and phosphoproteomic profiling of kidney tissues from APAP-treated mice to investigate the underlying molecular mechanisms and identify potential therapeutic targets. Ten-week-old male C57BL/6 mice were fasted overnight for 16 hours prior to APAP administration. AKI was induced by intraperitoneal injection of a high dose of APAP (300 mg/kg body weight) for 6 hours (n = 4), while control mice received an equivalent volume of PBS via intraperitoneal injection (n = 4). Kidney tissues were collected from both APAP-treated and control groups for downstream omics analyses.
2025-11-24 | PXD063122 | Pride
Project description:To study the global changes of liver transcriptome after acetaminophen overdose. To study the global changes of transcriptome in the liver after acetaminophen overdose. Eight week old female C57BL/6 mice were fasted for 24 hours prior to a single intraperitoneal injection of 350mg/kg of acetaminophen in phosphate buffer saline (PBS) (treatment group) or PBS (control group). The mice were euthanized at different time points post exposure; plasma and tissue samples were collected for pathological examination and biochemical analyses.
2013-05-03 | E-GEOD-42181 | biostudies-arrayexpress
Project description:To study the global changes of liver transcriptome after acetaminophen overdose. To study the global changes of transcriptome in the liver after acetaminophen overdose. Eight week old female C57BL/6 mice were fasted for 24 hours prior to a single intraperitoneal injection of 350mg/kg of acetaminophen in phosphate buffer saline (PBS) (treatment group) or PBS (control group). The mice were euthanized at different time points post exposure; plasma and tissue samples were collected for pathological examination and biochemical analyses.
2013-05-03 | E-GEOD-42178 | biostudies-arrayexpress
Project description:Acetaminophen (APAP) overdose can lead to acute kidney injury (AKI), yet its molecular mechanisms remain unclear and no effective treatments are currently available. In this study, we combined transcriptomic, proteomic, and phosphoproteomic profiling of kidneys from APAP-exposed mice to explore molecular mechanisms and potential therapeutic strategies. Ten-week-old male C57BL/6 mice were fasted overnight for 16 hours prior to APAP treatment. Acute kidney injury was induced by intraperitoneal injection of APAP overdose (300 mg/kg body weight) for 6 hours (n = 4). Control mice received an equivalent volume of PBS via intraperitoneal injection (n = 4). Kidney tissues were subsequently collected from APAP-induced kidney injury mice and PBS-injected controls.
2025-12-05 | PXD063126 | Pride
Project description:Differential gene expression in mice liver after carbon tetrachloride and acetaminophen administration. Livers from control mice were compared with drug treated mice livers at different time points. Keywords: Time-course
2007-02-27 | GSE4874 | GEO
Project description:Acetaminophen overdose is the most common cause of acute liver injury (ALI) or acute liver failure in the USA. Its pathogenetic mechanisms are incompletely understood. Additional studies are warranted to identify new genetic risk factors for more mechanistic insights and new therapeutic target discoveries. The objective of this study was to explore the role and mechanisms of nicotinamide phosphoribosyltransferase (NAMPT) in acetaminophen-induced ALI. C57BL/6 Nampt gene wild type (Nampt+/+)-, heterozygous knockout (Nampt+/-)-, and overexpression (NamptOE)-mice were treated with overdose of acetaminophen, followed by histological, biochemical, and transcriptomic evaluation of liver injury. The mechanism of Nampt in acetaminophen -induced hepatocytic toxicity was also explored in cultured primary hepatocytes. Three lines of evidence have convergently demonstrated that acetaminophen overdose triggers the most severe oxidative stress and necrosis, and the highest expression of key necrosis driving genes in Nampt+/- mice, while the effects in NamptOE mice were least severe relative to Nampt+/+ mice. These findings support that NAMPT protects against acetaminophen induced ALI.
2018-04-03 | GSE110787 | GEO
Project description:Acetaminophen-induced liver injury (AILI) occurs frequently and can be life threatening. Although AILI is mainly caused by the direct drug cytotoxicity, increasing evidence suggests that the interplay between hepatocytes and immune cells can define this pathogenic process. To further understand the immunoregulatory role of SRA in AILI, we performed RNA-sequencing analysis using hepatic nonparenchymal cells (NPCs) derived from acetaminophen treated WT or SRA-/- mice to demonstrate hepatocyte-extrinsic mechanisms governed by the immune receptor SRA that maintains liver homeostasis upon drug insult.
2023-12-23 | GSE221747 | GEO
Project description:Microarray of MDMX C462A and wildtype mice treated with acetaminophen
| PRJNA655235 | ENA
Project description:Acetaminophen can adversely affect the liver especially when overdosed. We used whole blood as a surrogate to identify genes as potential early indicators of an acetaminophen-induced response. In a clinical study, healthy human subjects were dosed daily with 4g of either acetaminophen or placebo pills for 7 days and evaluated over the course of 14 days. Alanine aminotransferase (ALT) levels for responders to acetaminophen increased between days 4 and 9 after dosing and 12 genes were detected with expression profiles significantly altered within 24hrs. The early responsive genes separated the subjects by class and dose period. In addition, the genes clustered patients who overdosed on acetaminophen apart from controls and also predicted the exposure classifications with 100% accuracy. The responsive genes serve as early indicators of an acetaminophen exposure and their gene expression profiles can potentially be evaluated as molecular indicators for further consideration. Overdosed patients admitted to the emergency room. Five male and female individuals from 19 - 59 years old were admitted to the emergency room following an overdose on acetaminophen. The patients presented 12hrs to 4 days after ingestion. ALT and AST elevated peaking beyond 400 U/I and 120 U/I. Blood was collected 2 or 5 days following ingestion.
2016-02-16 | E-GEOD-70786 | biostudies-arrayexpress