Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Objective: To observe the effects of paeoniflorin on the expressions of CTGF and PDGF in liver tissue of fibrosis and the serum level of TNF-alpha in mice infected with Schistosoma japonicum, and to explore the protective effect and its mechanisms of paeoniflorin on liver fibrosis.
Methods: Kunming mice were divided randomly into 5 groups, namely normal control group (Group A), paeoniflorin groups (Group B, C, D) and infected control group (Group E). The mice in Group B-E were infected with cercariae of Schistosoma japonicum, and then they were treated with praziquantel (400 mg/kg per day) for 2 days after 6 weeks. After that, the mice in Group B, C, D were given paeoniflorin with a dose of 30, 60, 120 mg/(kg x d), respectively. After 8 weeks of paeoniflorin treatment, all the mice were killed, and their livers and serum were obtained. Hematoxylin and eosin stain and Masson stain were used to observe the degree of hepatic fibrosis. Immunohistochemical staining was performed to detect the expressions of CTGF and PDGF in liver tissue. The serum level of TNF-alpha was detected by ELISA.
Results: The expression levels of CTGF and PDGF proteins in liver tissue and the serum level of TNF-alpha of the mice in the high dosage paeoniflorin treatment group (Group D) were significantly lower than those in the infected control group (P < 0.05).
Conclusions: The effects of paeoniflorin on hepatic fibrosis induced by Schistosoma japonicum infection depends on its dosage. Paeoniflorin may exert its effects by inhibiting the serum level of TNF-alpha and down regulating the expression of CTGF and PDGF proteins.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Modulation of Gene Expression in Human Fibroblasts by Punicalagin and Ellagic Acid: An In Vitro Study.
Mol Nutr Food Res
September 2025
Biomedical Group (BIO277), Department of Nursing, Faculty of Health Sciences, University of Granada, Granada, Spain.
The effects of the phenolic compounds punicalagin and ellagic acid, derived from pomegranate, were analyzed on the gene expression of cultured human fibroblasts. The focus was placed on genes associated with growth factors, differentiation markers, and extracellular matrix (ECM) components, all of which play a crucial role in effective wound healing. The human dermal fibroblast cell line CCD-1064Sk was used, and the bioactive compounds punicalagin and ellagic acid were administered to cultured fibroblasts at concentrations of 10 and 10 M, respectively.
View Article and Find Full Text PDFCircular RNAs in Organ Fibrosis.
Adv Exp Med Biol
August 2025
Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Fibrosis is an irreversible process that occurs in all major organs in the body; however, excessive fibrosis results in organ dysfunction and possible death. This process involves robust proliferation of fibroblasts and, in turn, excessive accumulation of extracellular matrix (ECM) within and around damaged tissues, leading to abnormal architectural remodeling (Cannito S, Novo E, Parola M, Adv Drug Deliv Rev 121:57-84, 2017; Kendall RT, Feghali-Bostwick CA, Front Pharmacol 5:123, 2014). The fibrotic process can be triggered and initiated by various fibrotic factors such as transforming growth factor-β (TGF-β) (Travis MA, Sheppard D, Annu Rev Immunol 32:51-82, 2014), members of the connective tissue growth factor (CTGF) family as well as the platelet-derived growth factor (PDGF) family (Wynn TA, J Pathol 214(2):199-210, 2008).
View Article and Find Full Text PDFThe fibrosis puzzle of systemic sclerosis-associated ILD and the quest for targeted interventions.
Ther Adv Respir Dis
August 2025
Academician Ye. M. Neiko Department of Internal Medicine #1, Clinical Immunology and Allergology, Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine.
Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is a leading cause of morbidity and mortality in systemic sclerosis, marked by complex immunopathogenic mechanisms and progressive fibrosis. Recent advances have illuminated key cellular players as T cells, macrophages, dendritic cells, and profibrotic mediators such as TGF-β, PDGF, and CTGF, alongside emerging roles for epigenetic reprogramming in sustaining fibroblast activation. This narrative review synthesizes current understanding of immune-fibrotic crosstalk and critically evaluates both established therapies (e.
View Article and Find Full Text PDFFibrotic Disease: from Signaling Pathways and Biomarkers to Molecular Imaging.
Mol Imaging Biol
August 2025
Pharmaceutical Sciences Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran.
Fibrotic diseases are characterized by excessive accumulation of extracellular matrix (ECM) components following tissue injury, ultimately leading to organ dysfunction and failure. The progression of fibrosis is governed by complex molecular signaling pathways, including TGF-β, PDGF, FGF, CTGF, VEGF, and many others, which regulate myofibroblast activation, ECM production, and tissue remodeling. Traditional diagnostic modalities such as magnetic resonance imaging (MRI), computed tomography (CT), and biopsy are limited in their ability to distinguish active fibrogenesis from established fibrosis or detect early molecular changes.
View Article and Find Full Text PDFElucidating the pathogenesis of oral submucous fibrosis: A comprehensive review.
Arch Oral Biol
October 2025
Bioprospection and Product Development Division, CSIR-Central Institute of Medicinal and Aromatic Plants, Near Kukrail Picnic Spot Road, Lucknow, Uttar Pradesh 226015, India. Electronic address:
Objective: Oral submucosal fibrosis (OSMF) is a progressive and potentially malignant disorder of the oral cavity. This review aims to explore the key mechanisms underlying OSMF pathogenesis and its malignant transformation to oral cancer, focusing on the role of associated cells, growth factors, and signaling pathways, by detailing the sequential events within each pathway and their interconnections.
Design: A comprehensive literature search was conducted using databases such as PubMed, Scopus, Google Scholar, and SciFinder to identify affected cells, pathways, and cellular mechanisms associated with OSMF and oral cancer.