The present study aimed to explore the treatment effects of Taohongsiwu decoction on the liver fibrosis in a rat model, as few prior studies have investigated the anti-fibrotic effects of Taohongsiwu decoction. High-performance liquid chromatography was used to measure the concentration of ferulic acid and hydrosafflower flavin A in the decoction. Male Sprague-Dawley rats were randomly divided into control, model, colchicine (positive group), Taohongsiwu-high, Taohongsiwu-moderate and Taohongsiwu-low groups; 50% carbon tetrachloride (CCl4) of peanut oil solution was subcutaneously injected to the rats except for the control group, and the drugs were intragastrically administered (10 ml/kg) starting at week 7 for 6 continuous weeks. The rats were deprived of food but not water for 12 h following the final administration, then blood was collected from the abdominal aorta. The liver tissues were obtained, fixed with 10% neutral formaldehyde, and embedded with paraffin. The concentrations of ferulic acid and hydroxysafflor flavin A in Taohongsiwu decoction were 0.12 and 0.57 mg/ml, respectively. The three groups treated with Taohongsiwu decoction were found with significantly lower serum levels of aspartate aminotransferase, alanine amino transferase, collagen IV and hyaluronic acid, as well as higher level of albumin (ALB); in addition, the expression levels of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) mRNA and collagen I were significantly downregulated. Taohongsiwu decoction improved the liver function, reduced the collagen deposition in the serum and liver tissues, and inhibited the expression of α-SMA and TGF-β1.
Salvianolic acid B (Sal B) has previously reported anti-hepatic fibrosis effects, though it is not clear if it can inhibit hepatic fibrosis by regulating the hedgehog (Hh) signaling pathway. The aim of the present study was to explore the roles and mechanism of Sal B in preventing and treating liver fibrosis in rats. The study also aimed to determine the role of the Hh signaling pathway in this process. A rat model of liver fibrosis was induced through the subcutaneous injection of 50% carbon tetrachloride, followed by treatment with Sal B. After gavage, blood was collected to detect serum markers of liver injury. The degree of liver fibrosis and tissue damage was assessed using histopathological analysis. Western blotting and reverse transcription-quantitative PCR were used to detect the expression levels of TGF-β1 and Hh signaling pathway-related genes, including Sonic hedgehog (Shh) protein, membrane protein receptor protein patched homolog 1 (Ptch1), membrane protein receptor Smoothened (Smo) and transcription factor glioma-associated oncogene homolog 1 (Gli1). Serum alanine aminotransferase, aspartate aminotransferase and total bilirubin levels were decreased, whilst levels of albumin were increased in rats with liver fibrosis that were treated with Sal B (P<0.05). Additionally, significant increases in TGF-β1, Shh, Ptch1, Smo, Gli1 and α-smooth muscle actin expression levels were observed in the liver tissues of rats with hepatic fibrosis (P<0.05). However, Sal B treatment significantly reduced the expression levels of these proteins (P<0.05). In conclusion, the results of the present study suggested that the Hh signaling pathway may be activated during the process of rat liver fibrosis. Thus, Sal B may exert its anti-hepatic fibrosis effects, at least in part, by inhibiting the activation of the Hh signaling pathway.
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