Paracetamol Poisoning: Epidemiology, Diagnosis, Treatment (Status of the Issue) DOI Creative Commons
В. Г. Сенцов,

K. Yu. Gusev,

Н. С. Давыдова

et al.

Ural Medical Journal, Journal Year: 2024, Volume and Issue: 23(6), P. 108 - 131

Published: Dec. 12, 2024

Introduction . Paracetamol (acetaminophen) is an over-the-counter analgesic and antipyretic drug, available in monoform included more than 200 combined drugs. Today, paracetamol widely used medicine, therefore different age categories, including children from 0 to 18 years old, adults, the elderly pregnant women. The aim systematize data on epidemiology, diagnosis treatment of poisoning based foreign domestic literature. Materials methods Literary search platforms PubMed, Google Scholar, eLibrary.ru, CyberLeninka by keywords “paracetamol, acetaminophen, poisoning, hepatotoxicity, N -acetylcysteine”. Inclusion criteria: original, review articles, randomized non-randomized clinical trials, meta-analyses systematic reviews topic poisoning. Results discussion literature presents toxic effects, metabolism, picture; modern research Conclusions. Modern diagnosing allow us focus not only determining concentration drug blood or dose taken orally, as a decision-making tool. development new biomarkers liver damage promising diagnostic tool, suggesting “early warning” potential damage.

Language: Английский

Endoplasmic Reticulum Stress and Mitochondrial Stress in Drug-Induced Liver Injury DOI Creative Commons

Sisi Pu,

Yangyang Pan,

Qian Zhang

et al.

Molecules, Journal Year: 2023, Volume and Issue: 28(7), P. 3160 - 3160

Published: April 2, 2023

Drug-induced liver injury (DILI) is a widespread and harmful disease closely linked to mitochondrial endoplasmic reticulum stress (ERS). Globally, severe drug-induced hepatitis, cirrhosis, cancer are the primary causes of liver-related morbidity mortality. A hallmark DILI ERS changes in morphology function, which increase production reactive oxygen species (ROS) vicious cycle mutually reinforcing responses. Several pathways maladapted maintain homeostasis during DILI. Here, we discuss processes caused by several types drugs that induce hepatocyte stress, focusing primarily on stress. Importantly, both mediated overproduction ROS, destruction Ca2+ homeostasis, unfolded protein response (UPR). Additionally, review new potential pharmacological targets for highlight possibilities treatment mitigation.

Language: Английский

Citations

27
Contribution of gut microbiota to drug-induced liver injury DOI
Huikuan Chu,

Yan Ai,

Zilu Cheng

et al.

Hepatobiliary & pancreatic diseases international, Journal Year: 2023, Volume and Issue: 22(5), P. 458 - 465

Published: June 15, 2023

Language: Английский

Citations

19
Evaluation of the Reparative Effect of Sinomenine in an Acetaminophen-Induced Liver Injury Model DOI Creative Commons
Ahmet KAYALI, Ejder Saylav Bora, Hüseyin Acar

et al.

Current Issues in Molecular Biology, Journal Year: 2024, Volume and Issue: 46(1), P. 923 - 933

Published: Jan. 21, 2024

Due to its rising global prevalence, liver failure treatments are urgently needed. Sinomenine (SIN), an alkaloid from sinomenium acutum, is being studied for liver-repair properties due Acetaminophen (APAP) overdose. SIN’s effect on APAP-induced hepatotoxicity in rats was examined histologically and biochemically. Three groups of 30 adult male Wistar were created: control, APAP-only, APAP + SIN. Histopathological biochemical analyses performed samples after euthanasia. SIN significantly protected against damage. Compared reduced cellular injury preserved hepatocellular architecture. The Group had lower ALT, MDA, GSH levels, protecting damage oxidative stress. also dose-dependent antioxidant properties. When examining critical regulatory proteins, partially restored Sirtuin 1 (SIRT1) levels. While BMP-7 levels unaffected, histopathological evidence hepatocyte percentages supported liver-restorative effect. repaired rats’ livers injury. This study suggests that may treat acute damage, warranting further research into long-term effects, optimal dosage, clinical applications. These findings aid liver-related emergency department interventions life-saving treatments.

Language: Английский

Citations

4
Wogonin Mitigates Acetaminophen-Induced Liver Injury in Mice through Inhibition of the PI3K/AKT Signaling Pathway DOI Creative Commons

Wenyingzi Zhao,

Huishan Luo,

Zelong Lin

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 332, P. 118364 - 118364

Published: May 18, 2024

Scutellaria baicalensis Georgi (SBG), a widely used traditional Chinese medicine, exhibits anti-inflammatory and antioxidant properties. Wogonin is one of the primary bioactive components SBG. Acetaminophen (APAP)-induced liver injury (AILI) represents prevalent form drug-induced damage primarily driven by inflammatory responses oxidative stress.

Language: Английский

Citations

4
Chitinase 3-like protein 1 deficiency ameliorates drug-induced acute liver injury by inhibition of neutrophil recruitment through lipocalin-2 DOI Creative Commons

Ji Hye Kim,

In Jun Yeo, Dong Ju Son

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 24, 2025

Chitinase-3-like protein 1 (Chi3l1) is a member of the mammalian Chitinase-like family, and several studies reported that Chi3l1 associated with various inflammatory diseases as well liver diseases. Acetaminophen (APAP) usually used for antipyretic drug, but its overdose induces acute injury (ALI). Several subsequent responses immune system play critical role in severity outcome APAP-induced ALI. In present study, we investigated mechanism during ALI using knock-out (KO) mice. We explored function APAP-injected KO mice sought proteins through biological research data program investigating mechanism. Liver histological analysis revealed was attenuated compared to wild-type (WT) observed neutrophil infiltration decreased WT To investigate this mechanism, potentially by mRNA sequencing correlation data. found lipocalin-2 (Lcn2) examined Chi3l1, Lcn2, their relationship model recombinant antibodies. Our results suggest deficiency ameliorates abrogating Lcn2-mediated liver.

Language: Английский

Citations

0
Chicken meat hydrolysate improves acetaminophen-induced liver injury by alleviating oxidative stress via modulation in Keap1/Nrf2/HO-1 signaling in BALB/c mice DOI Creative Commons
Vipul Wayal,

Zhuo-En Tsai,

Yu‐Hsuan Lin

et al.

Journal of Agriculture and Food Research, Journal Year: 2025, Volume and Issue: unknown, P. 101863 - 101863

Published: March 1, 2025

Language: Английский

Citations

0
Metabolic Reprograming of Macrophages: A New Direction in Traditional Chinese Medicine for Treating Liver Failure DOI Creative Commons
Junli Zhang, Na Li, Xiaoyu Hu

et al.

Journal of Immunology Research, Journal Year: 2024, Volume and Issue: 2024(1)

Published: Jan. 1, 2024

Acute liver failure (ALF) is a fulminant clinical syndrome that usually leads to multiple organ and high mortality. Macrophages play crucial role in the initiation, development, recovery of ALF. Targeting macrophages through immunotherapy holds significant promise as therapeutic strategy. These cells exhibit remarkable plasticity, enabling them differentiate into various subtypes based on changes their surrounding microenvironment. M1-type are associated with pro-inflammatory phenotype primarily rely predominantly glycolysis. In contrast, M2-type macrophages, which characterized by anti-inflammatory phenotype, obtain energy from oxidative phosphorylation (OXPHOS) fatty acid oxidation (FAO). Shifting macrophage metabolism glycolysis OXPHOS inhibits M1 activation promotes M2 activation, thereby exerting reparative effects. This study elucidates relationship between glucose reprograming an immunometabolism perspective. A comprehensive literature review revealed several signaling pathways may regulate polarization metabolism, including phosphatidyl-inositol 3-kinase/protein kinase B (PI3K/AKT), mammalian target rapamycin (mTOR)/hypoxia-inducible factor 1

Language: Английский

Citations

2
Isolation and characterization of a hepatoprotective polysaccharide from Lonicera caerulea L. var. edulis Turcz. ex Herd. fruit against APAP-induced acute liver injury mice DOI

Qianru Xiang,

Zijun Xia,

Hongji Liu

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 275, P. 133426 - 133426

Published: Aug. 1, 2024

Language: Английский

Citations

1
Label-Free Imaging Techniques to Evaluate Metabolic Changes Caused by Toxic Liver Injury in PCLS DOI Open Access
Svetlana Rodimova,

Artem M Mozherov,

Vadim Elagin

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(11), P. 9195 - 9195

Published: May 24, 2023

Abuse with hepatotoxic agents is a major cause of acute liver failure. The search for new criteria indicating the or chronic pathological processes still challenging issue that requires selection effective tools and research models. Multiphoton microscopy second harmonic generation (SHG) fluorescence lifetime imaging (FLIM) are modern label-free methods optical biomedical assessing metabolic state hepatocytes, therefore reflecting functional tissue. aim this work was to identify characteristic changes in hepatocytes precision-cut slices (PCLSs) under toxic damage by some most common toxins: ethanol, carbon tetrachloride (CCl4) acetaminophen (APAP), commonly known as paracetamol. We have determined damage, these turn out be specific each agent, underlying mechanisms toxicity. results obtained consistent standard molecular morphological analysis. Thus, our approach, based on imaging, intravital monitoring tissue case even cases injury.

Language: Английский

Citations

3
6-Hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline Demonstrates Anti-Inflammatory Properties and Reduces Oxidative Stress in Acetaminophen-Induced Liver Injury in Rats DOI Creative Commons
Е. Д. Крыльский,

Svetlana E. Kravtsova,

Т. Н. Попова

et al.

Current Issues in Molecular Biology, Journal Year: 2023, Volume and Issue: 45(10), P. 8321 - 8336

Published: Oct. 12, 2023

We examined the effects of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline on markers liver injury, oxidative status, and extent inflammatory apoptotic processes in rats with acetaminophen-induced damage. The administration acetaminophen caused accumulation 8-hydroxy-2-deoxyguanosine 8-isoprostane serum, as well an increase biochemiluminescence indicators. Oxidative stress resulted activation pro-inflammatory cytokine NF-κB factor mRNA synthesis increased levels immunoglobulin G, along higher activities caspase-3, caspase-8, caspase-9. also development stress, leading to a decrease level reduced glutathione imbalance function antioxidant enzymes. This study discovered that by its activity, hence reducing mRNA, decreasing concentration G. These changes reduction activity caspase-8 caspase-9, which are involved ligand-induced mitochondrial pathways apoptosis inhibited effector caspase-3. In addition, promoted normalization system animals treated acetaminophen. As result, compound being tested alleviated inflammation led improved marker indices ameliorated histopathological alterations.

Language: Английский

Citations

3