Anti-fibrotic effects of Cuscuta chinensis with in vitro hepatic stellate cells and a thioacetamide-induced experimental rat model

被引:21
作者
Kim, Jin Seoub [1 ,2 ]
Koppula, Sushruta [1 ,3 ]
Yum, Mun Jeong [1 ,4 ]
Shin, Gwang Mo [1 ]
Chae, Yun Jin [1 ]
Hong, Seok Min [5 ]
Lee, Jae Dong [6 ]
Song, MinDong [1 ,3 ]
机构
[1] Konkuk Univ, Grad Sch, Dept Appl Life Sci, Chungju Si, South Korea
[2] Univ Ulsan, Asan Inst Life Sci, Dept Infect Dis, Asan Med Ctr,Coll Med, Seoul, South Korea
[3] Konkuk Univ, Dept Biotechnol, Coll Biomed & Hlth Sci, Chungju Si, South Korea
[4] R&D Ctr Korean Drug Co Ltd, Seoul, South Korea
[5] Medrim Corp, Chungju Si, South Korea
[6] Konkuk Univ, Sch Med, Dept Internal Med, Chungju Si, South Korea
关键词
Glutathione; hydroxyproline; apoptosis; silymarin; aspartate; alanine; INDUCED LIVER FIBROSIS; FAT-STORING CELLS; RESIN GLYCOSIDE; TGF-BETA; EXPRESSION; PROLIFERATION; APOPTOSIS; ACTIVATION; MECHANISMS; SILYMARIN;
D O I
10.1080/13880209.2017.1340965
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context:Cuscuta chinensis Lam. (Convolvulaceae) has been used as a traditional herbal remedy for treating liver and kidney disorders. Objective: Anti-fibrotic effects of C. chinensis extract (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 (alpha-SMA, Col1 alpha 1 and TGF-beta 1) 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 and p < 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. In in vivo studies, 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.
引用
收藏
页码:1909 / 1919
页数:11
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