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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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Elucidating the Phase I metabolism of psilocin in vitro.

Arch Toxicol

January 2025

Department of Pharmacy and Pharmaceutical Sciences, National University of Singapore, 18 Science Drive 4, Singapore, 117543, Singapore.

Psilocin is a well-studied controlled substance with potential psychotherapeutic applications. However, research gaps remain regarding its metabolism. Our objective was to elucidate a comprehensive Phase I metabolic profile of psilocin to support its forensic management and clinical development.

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Apigenin (CHO, API) is a natural flavonoid widely found in vegetables, fruits, and plants such as celery, oranges, and chamomile. In recent years, API has attracted considerable attention as a dietary supplement due to its low toxicity, non-mutagenic properties and remarkable therapeutic efficacy in various diseases. In particular, evidence from a large number of preclinical studies suggests that API has promising effects in the prevention and treatment of a variety of liver diseases, including multifactorial liver injury, non-alcoholic fatty liver disease/non-alcoholic steatohepatitis, liver fibrosis and liver cancer.

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Since the establishment of the COVID-19 pandemic, a range of studies have been developed to understand the pathogenesis of SARS-CoV-2 infection, vaccine development, and therapeutic testing. However, the possible impacts that these viruses can have on non-target organisms have been explored little, and our knowledge of the consequences of the COVID-19 pandemic for biota is still very limited. Thus, the current study aimed to address this knowledge gap by evaluating the possible impacts of oral exposure of C57Bl/6 J female mice to SARS-CoV-2 lysate protein (at 20 µg/L) for 30 days, using multiple methods, including behavioral assessments, biochemical analyses, and histopathological examinations.

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Sulfonated albumin from hepatocytes accelerates liver fibrosis in nonalcoholic fatty liver disease through endoplasmic reticulum stress.

Free Radic Biol Med

December 2024

Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250021, Shandong, China; Department of Infectious Disease, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, Shandong, China. Electronic address:

Article Synopsis
  • The study investigates the role of sulfonated albumin as a modification in nonalcoholic fatty liver disease (NAFLD), focusing on its sources and effects on liver fibrosis.
  • Researchers found higher levels of sulfonated albumin in both human and mouse serum samples with NAFLD, and its injection in mice worsened liver conditions.
  • The mechanism involves hepatocyte-derived sulfonated albumin activating hepatic stellate cells through the GAL3 receptor, promoting liver fibrosis and suggesting its potential as a diagnostic marker and treatment target for NAFLD.
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