Background: Tea polyphenols have been shown to protect against carbon tetrachloride (CCl4)-induced liver injury, liver fibrosis, hepatic ischemia-reperfusion injury. In this study, we examined the effect of tea polyphenols on lipopolysaccharide (LPS)-induced liver injury, and explored its mechanisms.
Methods: Sprague-Dawley rats received tea polyphenols (100 mg.kg-1.d-1) or vehicle (water) intragastrically by gavage for 14 days, followed by LPS (5 mg/kg) or saline injection intraperitoneally. Liver injury was assessed by biochemical assay and pathological analysis. Serum tumor necrosis factor-alpha (TNF-alpha) levels and liver malondialdehyde (MDA) contents were determined. Inducible nitric oxide synthase (iNOS) protein and TNF-alpha, iNOS and endothelial nitric oxide synthase (eNOS) mRNA expressions in the liver were detected by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR), respectively.
Results: Administration of LPS resulted in liver injury in rats, evidenced by elevated activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), hepatocellular necrosis, and neutrophil infiltration in the liver. These responses were associated with increased serum TNF-alpha levels, induced iNOS protein, expressions of TNF-alpha, iNOS mRNA in the liver and elevated lipid peroxidation at 90 minutes or 6 hours after LPS injection. Pretreatment with tea polyphenols attenuated LPS-induced liver injury, and blunted the rises of serum TNF-alpha levels and lipid peroxidation and the induction of expressions of TNF-alpha, iNOS in the liver.
Conclusion: Tea polyphenols prevent LPS-induced liver injury, and the mechanisms may involve the reduction of serum TNF-alpha levels and lipid peroxidation and the suppression of TNF-alpha, iNOS expressions in the liver.
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Sickle cell disease (SCD) is the most common genetic disease in the world and a societal challenge. SCD is characterized by multi-organ injury related to intravascular hemolysis. To understand tissue-specific responses to intravascular hemolysis and exposure to heme, we present a transcriptomic atlas in the primary target organs of HbSS vs HbAA transgenic SCD mice.
View Article and Find Full Text PDFWhile key for pathogen immobilization, neutrophil extracellular traps (NETs) often cause severe bystander cell/tissue damage. This was hypothesized to depend on their prolonged presence in the vasculature, leading to cytotoxicity. Imaging of NETs (histones, neutrophil elastase, extracellular DNA) with intravital microscopy in blood vessels of mouse livers in a pathogen-replicative-free environment (endotoxemia) led to detection of NET proteins attached to the endothelium for months despite the early disappearance of extracellular DNA.
View Article and Find Full Text PDFEur J Anaesthesiol
January 2025
From the Department of Anaesthesia, King's College Hospital NHS Foundation Trust, London, UK (BM, GK), Institute of Liver Studies, King's College Hospital NHS Foundation Trust, London, UK (KM, MM), Department of Critical Care, Guy's & St Thomas' NHS Foundation Trust, London, UK (MO), Department of Critical Care, University of Pittsburgh, USA (JAK), School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, UK (GK).
J Am Coll Surg
January 2025
Division of Trauma & Surgical Critical Care, DeWitt Daughtry Family Department of Surgery, Ryder Trauma Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Background: Venous thromboembolism (VTE) remains a major source of morbidity and mortality in severely injured patients despite current methods of risk stratification and prophylaxis, suggesting incomplete understanding of VTE risk factors. Given the liver's role in coagulation, we hypothesized that liver injury (LI) is associated with increased rates of VTE in severely injured patients.
Study Design: The American College of Surgeons Trauma Quality Improvement Project database (TQIP) 2017-2021 was retrospectively reviewed for patients with a maximum abdominal Abbreviated Injury Score (AIS) ≥ 4 with or without LI.
Liver Int
February 2025
Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Aim: This research was aimed to uncover the hepatitis B virus (HBV) and hepatitis C virus (HCV) related diseases burden in Asia over the past 3 decades, estimating from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019.
Methods: Age-standardised rates, case numbers of prevalence, disability-adjusted life-years (DALYs), incidence and deaths with 95% uncertainty intervals (UI) for HBV/HCV-related diseases from 1990 to 2019 were derived from GBD 2019 database, with the estimated annual percentage changes (EAPCs) calculated. Our analysis also encompassed the association between the Sociodemographic Index (SDI) and the burden of HBV/HCV-related diseases, future disease burden predictions in six selected countries and various risk factors.
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