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26-Week Repeated-Dose Toxicity Study of a Novel Antiarrhythmic Drug Sulcardine Sulfate in Sprague-Dawley Rats.
J Appl Toxicol
January 2025
School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing, China.
Sulcardine sulfate (Sul) is a novel antiarrhythmic agent blocking multiple channels and exhibits unique pharmacological properties such as lower APD-dependent prolongation and reduced arrhythmia risk. Sul is currently in Phase III clinical trials, yet studies on its long-term toxicological profile and potential target organs remain unexplored. This study investigated the related toxicity of Sul in Sprague Dawley (SD) rats through repeated oral administration for 26 weeks, followed by a 4-week recovery period.
View Article and Find Full Text PDFResveratrol attenuates cyclophosphamide-induced hepatic apoptosis in association with the inhibition of oxidative stress and inflammation in a rat model of acute liver injury.
Tissue Cell
January 2025
Department of Medical Laboratory, College of Applied Medical Sciences, Prince Sattam bin Abdulaziz University, Al-Kharj 11942, Saudi Arabia.
Cyclophosphamide (CP) is an alkylating chemotherapy agent that induces liver toxicity by cross-linking DNA, causing cell apoptosis. While CP is effective in cancer treatment, its side effects on the liver are significant. Recent studies have indicated that antioxidants, such as resveratrol, may reduce these toxic effects.
View Article and Find Full Text PDFThe C3/C3aR pathway exacerbates acetaminophen-induced mouse liver injury via upregulating podoplanin on the macrophage.
FASEB J
January 2025
Jiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Suzhou, China.
Acute liver failure (ALF) is a life-threatening condition that occurs when the liver sustains severe damage and rapidly loses its function. The primary cause of ALF is the overdose of acetaminophen (APAP), and its treatment is relatively limited. The involvement of the complement system in the development of ALF has been implicated.
View Article and Find Full Text PDFInduction of MASH in three-dimensional bioprinted human liver tissue.
PLoS One
January 2025
University of California, San Diego, La Jolla, California, United States of America.
Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (MASH), is a major risk factor for cirrhosis and hepatocellular carcinoma (HCC) and a leading cause of liver transplantation. MASH is caused by an accumulation of toxic fat molecules in the hepatocyte which leads to inflammation and fibrosis. Inadequate human "MASH in a dish" models have limited our advances in understanding MASH pathogenesis and in drug discovery.
View Article and Find Full Text PDFComplement 3a receptor 1 on macrophages and Kupffer cells is not required for the pathogenesis of metabolic dysfunction-associated steatotic liver disease.
Elife
January 2025
Division of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Together with obesity and type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global epidemic. Activation of the complement system and infiltration of macrophages has been linked to progression of metabolic liver disease. The role of complement receptors in macrophage activation and recruitment in MASLD remains poorly understood.
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