Protective effects of Ampelopsis brevipedunculata against in vitro hepatic stellate cells system and thioacetamide-induced liver fibrosis rat model

被引:17
作者
Yum, Mun Jeong [1 ,2 ]
Koppula, Sushruta [1 ,3 ]
Kim, Jin Seoub [1 ]
Shin, Gwang Mo [1 ]
Chae, Yun Jin [3 ]
Yoon, Tony [4 ]
Chun, Chi Su [4 ]
Lee, Jae Dong [5 ]
Song, MinDong [1 ,3 ]
机构
[1] Konkuk Univ, Dept Appl Life Sci, Grad Sch, Chungju Si 27478, Chungcheongbuk, South Korea
[2] Ctr Korean Drug Co Ltd, R&D Ctr, Seoul, South Korea
[3] Konkuk Univ, Coll Biomed & Hlth Sci, Dept Biotechnol, Chungju Si, Chungcheongbuk, South Korea
[4] Food One Corp, Deoksan Myeon Jincheon G, Chungcheongbuk, South Korea
[5] Konkuk Univ, Sch Med, Dept Internal Med, Chungju, Chungbuk, South Korea
关键词
Extracellular matrix; glutathione; hydroxyproline; apoptosis; reactive oxygen species; silymarin; FAT-STORING CELLS; VITACEAE; MICE; HYDROXYPROLINE; FIBROGENESIS; ANTIOXIDANT; PROGRESSION; SILYMARIN; CIRRHOSIS; REVERSAL;
D O I
10.1080/13880209.2017.1311928
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Context: Ampelopsis brevipedunculata Maxim (Vitaceae) is a traditional medicinal herb used for treating liver disorders. Objective: The hepatoprotective effects of A. brevipedunculata ethanol extract (ABE) was investigated in experimental models of fibrosis. Materials and methods: Hepatic stellate cells (HSCs) system in vitro and thioacetamide (TAA)-induced liver fibrosis rat model in vivo were 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 (200mg/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-beta, alpha-SMA and Col1A1) in HSC-T6 cells were significantly (p<0.01) downregulated in ABE-treated groups compared with control group. In in vivo studies, ABE (10 and 100 mg/kg) treatment ameliorated the altered levels of serum biomarkers significantly (p<0.01 and p<0.001) in TAA-induced groups. Further, ABE (10 and 100mg/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.
引用
收藏
页码:1577 / 1585
页数:9
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