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The hepatoprotective effects of the polyphenol-enriched n-butanol fraction of against carbon tetrachloride-induced liver fibrosis in rats: study.
Toxicol Rep
June 2025
Department of Pharmacology and Toxicology, College of Pharmacy, Al-Nahrain University, Baghdad, Iraq.
Liver fibrosis is a continuous wound-healing response to chronic injury caused by various chemical, virus, and pathological disorders; the lack of approved drugs or methods to reverse or prevent liver fibrosis makes it an interesting area of research. This study investigates the potential hepatoprotective effects of the phenolic extract of in rat's module of liver fibrosis. Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl) for six consecutive weeks; the butanol fraction of and silymarin was administered orally concurrently with CCl.
View Article and Find Full Text PDFAnalysis of serum concentrations of metoprolol and its metabolite α-hydroxymetoprolol in patients with heart failure with reduced ejection fraction: a pilot study in routine health care.
Expert Rev Clin Pharmacol
January 2025
Department of Internal Medicine and Cardiology, University Hospital Ostrava, Ostrava, Czech Republic.
Background: The cardioselective β-1 receptor antagonist metoprolol is used to treat heart failure. It is metabolized in the liver, primarily by cytochrome 2D6.
Research Design And Methods: In this study, trough serum concentrations of metoprolol and its metabolite α-hydroxymetoprolol were measured in patients with heart failure with reduced ejection fraction.
Lack of fibro-inflammatory response in human mammary adipose tissue in obesity.
Int J Obes (Lond)
December 2024
Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, Université Toulouse III-Paul Sabatier (UT3), Toulouse, France.
Background: Understanding how obesity impacts human mammary adipose tissue (MAT) biology is crucial for deciphering its role in mammary epithelium during both physiological and pathophysiological processes, including breast cancer. Hypertrophic mammary adipocytes and Crown-Like Structures are present in MAT of patients with obesity but whether these changes initiate a fibro-inflammatory response at the tissue level remains insufficiently explored.
Objective: We investigated the markers of adipose tissue dysfunction (immune cell infiltration, secretion pattern and fibrosis) in tumor-free MAT of patients with obesity versus patients who are lean.
Investigating the mechanism of Tongfeng Qingxiao Formula for improving gouty arthritis based on the neutrophil extracellular trapping network.
J Ethnopharmacol
December 2024
Hospital Affiliated to Jiangxi University of Chinese Medicine, Nanchang, 330006, China; Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530011, China. Electronic address:
Ethnopharmacological Relevance: Traditional Chinese Medicine (TCM) has a history of thousands of years in China. The Tongfeng Qingxiao Formula (TFQXF), after decoction and oral administration, has shown significant therapeutic effects on Gouty arthritis (GA). TCM is often considered an experiential medicine, lacking modern scientific research, and the efficacy of TFQXF faces the same issue.
View Article and Find Full Text PDFSIRT1 Activation Suppresses Corneal Endothelial-Mesenchymal Transition via the TGF-β/Smad2/3 Pathway.
Curr Issues Mol Biol
December 2024
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.
Endothelial-mesenchymal transition (EnMT) is the transversion of endothelial cells to mesenchymal cells under certain physiological or pathological conditions. When EnMT occurs in the corneal endothelium, corneal endothelial cells (CECs) lose their normal function and thus cannot maintain corneal clarity. Studies have shown that the mechanism of EnMT in CECs involves the transforming growth factor-β (TGF-β) signaling pathway, and one of the important inhibitors of the TGF-β/Smad2/3 pathway is sirtuin-1 (SIRT1).
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