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Context:Cuscuta chinensisLam. (Convolvulaceae) has been used as a traditional herbal remedy for treating liver and kidney disorders. Objective:Anti-fibrotic effects ofC. chinensisextract (CCE) in cellular and experimental animal models were investigated. Materials and methods:HSC-T6 cell viability, cell cycle and apoptosis were analysed using MTT assay, flow cytometry and Annexin V-FITC/PI staining techniques. Thioacetamide (TAA)-induced fibrosis model was established using Sprague Dawley rats (n = 10). Control, TAA, CCE 10 (TAA with CCE 10 mg/kg), CCE 100 (TAA with CCE 100 mg/kg) and silymarin (TAA with silymarin 50 mg/kg). Fibrosis was induced by TAA (200 mg/kg,i.p.) twice per week for 13 weeks. CCE and silymarin were administered orally two times per week from the 7th to 13th week. Fibrotic related gene expression (α-SMA, Col1α1 and TGF-β1) was measured by RT-PCR. Serum biomarkers, glutathione (GSH) and hydroxyproline were estimated by spectrophotometer using commercial kits. Results:CCE (0.05 and 0.1 mg/mL) and silymarin (0.05 mg/mL) treatment significantly (p < 0.01 andp < 0.001) induced apoptosis (11.56%, 17.52% for CCE; 16.50% for silymarin, respectively) in activated HSC-T6 cells, compared with control group (7.26%). Further, rat primary HSCs showed changes in morphology with CCE 0.1 mg/mL treatment. Inin vivostudies, CCE (10 and 100 mg/kg) treatment ameliorated the TAA-induced altered levels of serum biomarkers, fibrotic related gene expression, GSH, hydroxyproline significantly (p < 0.05–0.001) and rescued the histopathological changes. Conclusions:CCE can be developed as a potential agent in the treatment of hepatofibrosis. [ABSTRACT FROM PUBLISHER]

Context:Ampelopsis brevipedunculataMaxim (Vitaceae) is a traditional medicinal herb used for treating liver disorders. Objective:The hepatoprotective effects ofA. brevipedunculataethanol extract (ABE) was investigated in experimental models of fibrosis. Materials and methods:Hepatic stellate cells (HSCs) systemin vitroand thioacetamide (TAA)-induced liver fibrosis rat modelin vivowere used. Sprague–Dawley rats were divided into five groups of eight each (control, TAA, TAA with ABE 10 mg/kg, ABE 100 mg/kg and silymarin 50 mg/kg groups, respectively). Fibrosis was induced except to the control group by TAA (200 mg/kg, i.p.) twice per week for 13 weeks. ABE and silymarin was administered orally six times per week from the 7th week to the 13th week. Results:In HSC-T6 cells, ABE (0.1 mg/mL) and silymarin (0.05 mg/mL) significantly (p < 0.01) induced apoptosis (12.94 ± 5.72% and 14.9 ± 3.8%, respectively) compared with control group (7.51 ± 1.26%). The expression of fibrosis related genes (TGF-β, α-SMA and Col1A1) in HSC-T6 cells were significantly (p < 0.01) downregulated in ABE-treated groups compared with control group. Inin vivostudies, ABE (10 and 100 mg/kg) treatment ameliorated the altered levels of serum biomarkers significantly (p < 0.01 andp < 0.001) in TAA-induced groups. Further, ABE (10 and 100 mg/kg) significantly (p < 0.01) attenuated the altered histopathological findings, glutathione content and the accumulation of hydroxyproline. Conclusion:These results collectively indicate that ABE can potentially be developed as a therapeutic agent in the treatment of hepatic fibrosis. [ABSTRACT FROM PUBLISHER]