Protective effects of Ampelopsis brevipedunculata against in vitro hepatic stellate cells system and thioacetamide-induced liver fibrosis rat model.
Protective effects of Ampelopsis brevipedunculata against in vitro hepatic stellate cells system and thioacetamide-induced liver fibrosis rat model.
复制标题
DOI：
10.1080/13880209.2017.1311928
复制
发表时间：
2017-12
影响因子：
3.8
通讯作者：
Song M
中科院分区：
文献类型：
--
作者：
Yum MJ;Koppula S;Kim JS;Shin GM;Chae YJ;Yoon T;Chun CS;Lee JD;Song M
背景：蛇葡萄为葡萄科植物，为治疗肝病的传统中草药。目的：在实验性肝纤维化模型上观察短梗参醇提物(ABE)的保肝作用。材料和方法：采用体外肝星状细胞系统和体内硫代乙酰胺诱导的大鼠肝纤维化模型。将SD大鼠随机分为5组，每组8只，每组8只，每组8只。每组8只，分别给予ABE 10 mg/kg、ABE 100 mg/kg和水飞蓟素50 /kg。除对照组外，TAA(2 0 0 mg/kg，i.p)均可致大鼠肝纤维化。每周两次，共13个 周。从第7周至第13周，安倍和水飞蓟素每周口服6次。结果：ABE(0.1 mg/m L)和水飞蓟素(0.0 5 m g/m L)诱导HSC-T6细胞凋亡(p <； 0.0 1)分别为12.94 ± 5.72%和14.9 ± 3.8%，而对照组为7.5 1 ± 1.2 6%。与对照组相比，ABE处理组肝细胞纤维化相关基因β，α-SMA和COL1A1的表达显著下调(p <； )。在体内实验中，ABE(10和100 mg/kg)治疗能显著改善TAA诱导组小鼠血清生物标志物的变化(p <； 0.001和p <； 100)。此外，ABE(10和100 mg/kg)显著减轻了组织病理学改变、谷胱甘肽含量和羟脯氨酸的积累(p <； 0.01)。结论：ABE有可能成为治疗肝纤维化的药物。
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 (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. 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 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.