Objective: To explore the effect of Dahuang Zhechong Pill (DHZCP) on transforming growth factor-beta 1 (TGF-beta 1) in rats hepatic stellate cells.
Methods: Liver fibrosis model rats were induced by CCl4 compound factor, and treated with DHZCP in three different dosages (ordinary, double and triple) separately. TGF-beta 1 and alpha-smooth muscle actin (alpha-SMA) synthesis expression, and grades of fibrosis were observed.
Results: TGF-beta 1 and alpha-SMA expression in the group treated with ordinary dose of DHZCP was insignificantly different from those in the control group (P > 0.05), but the expression attenuated significantly after treatment with double or triple dose of DHZCP in the portal area and discontinuous fibrous septum (P < 0.05, P < 0.01).
Conclusion: DHZCP of larger dosage could inhibit the hepatic stellate cells proliferation and secretion of TGF-beta 1, and reduce the genesis of collagen, so as to weaken the auto-secretion amplifying response of the cells, which might be one of the chief mechanisms of DHZCP in antagonizing liver fibrosis.
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Unlabelled: Metabolic syndrome and excessive alcohol consumption result in liver injury and fibrosis, which is characterized by increased collagen production by activated Hepatic Stellate Cells (HSCs). LARP6, an RNA-binding protein, was shown to facilitate collagen production. However, LARP6 expression and functionality as a regulator of fibrosis development in a disease relevant model remains elusive.
View Article and Find Full Text PDFLiver Int
February 2025
Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Background And Aims: Maternal obesity increases the risk of the paediatric form of metabolic dysfunction-associated steatotic liver disease (MASLD), affecting up to 30% of youth, but the developmental origins remain poorly understood.
Methods: Using a Japanese macaque model, we investigated the impact of maternal Western-style diet (mWSD) or chow diet followed by postweaning WSD (pwWSD) or chow diet focusing on bile acid (BA) homeostasis and hepatic fibrosis in livers from third-trimester fetuses and 3-year-old juvenile offspring.
Results: Juveniles exposed to mWSD had increased hepatic collagen I/III content and stellate cell activation in portal regions.
Int Immunopharmacol
January 2025
Liver fibrosis is a persistent damage repair response triggered by various etiological factors, resulting in an excessive accumulation of extracellular matrix (ECM). Activated hepatic stellate cells (HpSCs) are the primary source of ECM proteins. Therefore, specifically targeting HpSCs has become a crucial approach for treating liver fibrosis.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
College of Pharmacy and Food, Southwest Minzu University, Chengdu 610093, China.
Hepatic fibrosis (HF) is an important pathological state in the progression of chronic liver disease to end-stage liver disease and is usually triggered by alcohol, nonalcoholic fatty liver, chronic hepatitis viruses, autoimmune hepatitis (AIH), or cholestatic liver disease. Research on novel therapies has become a hot topic due to the reversibility of HF. Research into the molecular mechanisms of the pathology of HF and potential drug screening relies on reliable and rational biological models, mainly including animals and cells.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Laboratory of Nutritional Biochemistry, National Institute of Gastroenterology IRCCS "Saverio de Bellis", 70013 Castellana Grotte, Italy.
Navelina oranges () are rich in phytonutrients and bioactive compounds, especially flavonoids like hesperidin. This study investigates the anti-inflammatory and anti-fibrotic properties of hesperidin (HE) and a polyphenol mixture from Navelina oranges (OE) in human hepatocytes (Hepa-RG) and hepatic stellate cells (LX-2), in order to elucidate the underlying molecular mechanisms. In Hepa-RG cells, HE treatment increased expression of cannabinoid receptor 2 (CB2R), which was associated with down-regulation of p38 mitogen-activated protein kinases (p38 MAPK) but had minimal impact on cyclooxygenase-2 (COX-2) and transforming growth factor-β (TGF-β) levels.
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