Liver injury is a serious threat to human health, and γ-glutamyltranspeptidase (GGT) is proven to be one of the clinical biomarkers of liver injury. The conventional detection method of GGT activity in serum suffers from the complex operation, expensive equipment, and incapability of dynamically monitoring in biological samples. Herein, in consideration of the excellent characteristics of fluorescent probes, such as simple operation, high sensitivity, low cost, and good biocompatibility, a novel fluorescence detection method for GGT based on the combination of probe Rho-GGT and glutamic acid 5-hydrazide (glutamlhydrine) was designed. This method was applied to liver injury model mice to construct the relationship between the fluorescence signal, GGT activity, and the occurrence or development stage of liver injury. The fluorescence detection method combined with clinical indexes could more accurately characterize the situation of liver fibrosis, and evaluate the efficacy of liver fibrosis drugs, which could help provide important information for accurate diagnosis and early treatment of liver injury. The successful implementation of this project would promote the accurate in situ detection of GGT in liver injury, which was expected to guide pre-clinical diagnosis and clinical practice.
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http://dx.doi.org/10.1016/j.bios.2022.114767 | DOI Listing |
Alcohol Clin Exp Res (Hoboken)
January 2025
Department of Anatomy, Yonsei University Wonju College of Medicine, Wonju, Korea.
Background: Therapeutic options for managing intestinal and hepatic inflammation associated with alcohol consumption, a prevalent health problem worldwide, remain unavailable. This study examines the potential efficacy of polyethylene glycol (PEG) in mitigating the intestinal and hepatic damage, employing a mouse model for assessment.
Methods: First, the mixture of ethanol (4 g/kg body weight) and PEG (2 g/kg body weight) or an equivalent volume of vehicle was administered orally alcohol consumption.
J Clin Gastroenterol
December 2024
Department of Infectious Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Aim: To compare the respective clinical and pathologic features of antimitochondrial antibodies-negative (AMA-negative) primary biliary cirrhosis (PBC) and cholestatic type drug-induced liver injury (DILI) for clinical differential diagnosis.
Patients And Methods: Clinical data from 23 patients with AMA-negative PBC and 39 patients with cholestatic type DILI, treated at our hospital between January 2013 and January 2024, were collected and retrospectively analyzed.
Results: The cholestatic type DILI group exhibited a higher incidence of malaise and abdominal pain compared with the AMA-negative PBC group.
Hepatol Commun
November 2024
Human Immunology Laboratory, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
Background: HCC develops in the context of chronic inflammation; however, the opposing roles the immune system plays in both the development and control of tumors are not fully understood. Mapping immune cell interactions across the distinct tissue regions could provide greater insight into the role individual immune populations have within tumors.
Methods: A 39-parameter imaging mass cytometry panel was optimized with markers targeting immune cells, stromal cells, endothelial cells, hepatocytes, and tumor cells.
Hepatol Commun
November 2024
Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Background: Overdose of acetaminophen (APAP), a commonly used antipyretic analgesic, can lead to severe liver injury and failure. Current treatments are only effective in the early stages of APAP-induced acute liver injury (ALI). Therefore, a detailed examination of the mechanisms involved in liver repair following APAP-induced ALI could provide valuable insights for clinical interventions.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
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