Epigallocatechin gallate (EGCG), a major component of green tea extracts, is known to have anti-fibrotic properties in many organs. The aim of present study was to investigate effects of EGCG on rat pancreatic fibrosis induced by diethyldithiocarbamate (DDC). Oral gavages of different dose of EGCG (50, 100 and 200 mg/kg daily for 8 weeks) ameliorated histological changes and significantly suppressed collagen deposition in a dose-dependent manner. Meanwhile, administration of EGCG inhibited overexpression of TGF-beta1 and alpha-smooth muscle actin (a symbol of activation of pancreatic stellate cells). Moreover, EGCG has a potent influence on expression of Smads (downstream transcription factor of TGF-beta1). EGCG suppressed the expression of Smad3 and enhanced the expression of Smad7. In conclusion, our results demonstrated that EGCG attenuated rat pancreatic fibrosis induced by DDC and therefore may be an anti-fibrogenic candidate in the pancreatic fibrosis.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1248/bpb.30.1091 | DOI Listing |
Hepatol 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.
View Article and Find Full Text PDFJ Gastroenterol
January 2025
Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Unlabelled: Neonatal screening has been implemented internationally with different protocols and has become the routine method in the preclinical stage. Late diagnosis is associated with more severe symptoms with decreased survival and higher treatment costs.
Objectives: To estimate the incidence of cystic fibrosis; to evaluate the performance of the screening algorithms Immunoreactive Trypsinogen and Pancreatitis-Associated Protein (IRT/PAP) and the IRTxPAP product; to analyze the cut-off value for IRT, PAP, and IRTxPAP, and to establish a methodology for its ongoing evaluation; finally, to evaluate the quality of IRT and PAP measurements.
Genes Dis
March 2025
Department of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing 400038, China.
Pdgfrα stromal cells are a group of cells specifically expressing Pdgfrα, which may be mentioned with distinct names in different tissues. Importantly, the findings from numerous studies suggest that these cells share exactly similar biomarkers and properties, show complex functions in regulating the microenvironment, and are critical to tissue regeneration, repair, and degeneration. Comparing the similarities and differences between distinct tissue-resident Pdgfrα stromal cells is helpful for us to more comprehensively and deeply understand the behaviors of these cells and to explore some common regulating mechanisms and therapeutical targets.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Transplantation Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin Province 130061, China. Electronic address:
Chronic hepatitis B virus (HBV) infection is a major risk factor for liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Despite advances in understanding HBV-related liver diseases, effective therapeutic strategies remain limited. Macrophage migration inhibitory factor (MIF) has been implicated in various inflammatory and fibrotic conditions, but its role in HBV-induced liver fibrosis has not been fully explored.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!