目的:研究湖北海棠叶总黄酮对四氯化碳(CCl4)所诱导的大鼠肝纤维化的影响,并探讨其可能的作用机制。方法:腹腔注射2ml/kg CCl4橄榄油溶液制备大鼠肝纤维化模型。首次注射后分别灌胃给药湖北海棠叶总黄酮120mg/kg和60mg/kg,每天一次,共8周。测定血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、透明质酸、羟脯氨酸、β1-转化生长因子以及肝组织中总抗氧化能力、丙二醛含量和总超氧化物歧化酶的活性;用免疫组化方法定量肝组织中α-平滑肌肌动蛋白的表达。结果:与模型组比较,湖北海棠叶总黄酮能够调低血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、透明质酸、羟脯氨酸、β1-转化生长因子含量,降低肝组织丙二醛含量,增加肝组织中总抗氧化能力和总超氧化物歧化酶活性,降低α-平滑肌肌动蛋白的表达;病理学切片显示湖北海棠叶总黄酮能明显减轻CCl4引起的大鼠肝损伤及纤维化程度。结论:湖北海棠叶总黄酮在实验的120mg/kg和60mg/kg两个剂量组对CCl4致大鼠肝纤维化都有防治作用,作用机制可能与其抗氧化作用有关,湖北海棠叶总黄酮能能增强组织抗氧化能力,降低CCl4引起的脂类过氧化,保护细胞膜免受损伤,抑制β1-转化生长因子等具有加重肝纤维化程度的生物因子的表达,减轻肝纤维化程度。 Objective: To study the effect of total flavonoids from Begonia caulis L. on hepatic fibrosis induced by carbon tetrachloride (CCl4) in rats and to explore its possible mechanism. Methods: Rat model of hepatic fibrosis was established by intraperitoneal injection of 2ml / kg CCl4 olive oil solution. After the first injection, the total flavonoids of Begonia officinalis in Hubei were administered orally 120mg / kg and 60mg / kg, once daily for 8 weeks. Serum alanine aminotransferase, aspartate aminotransferase, hyaluronic acid, hydroxyproline, β1-transforming growth factor and total antioxidant capacity, malondialdehyde content and total superoxide dismutase Enzyme activity; immunohistochemistry method to quantify the α-smooth muscle actin expression in liver tissue. Results: Compared with the model group, the total flavonoids in Begonia caulis L. could reduce the content of serum alanine aminotransferase, aspartate aminotransferase, hyaluronic acid, hydroxyproline and β1-transforming growth factor, Malondialdehyde content, increase the total antioxidant capacity and total superoxide dismutase activity in liver tissue, reduce the expression of α-smooth muscle actin; pathological sections showed that the total flavonoids of Begonia officinalis leaves could significantly reduce the CCl4-induced rat liver Injury and fibrosis. CONCLUSION: The total flavonoids of Begonia cauliflower in Hubei could prevent and treat liver fibrosis induced by CCl4 in both the 120mg / kg and 60mg / kg experimental groups, and its mechanism may be related to its anti-oxidant effect. Enhance tissue antioxidant capacity, reduce the lipid peroxidation caused by CCl4, protect the cell membrane from injury, inhibit the expression of biological factors such as β1-transforming growth factor (TGF-β1) with aggravating degree of hepatic fibrosis, and reduce the degree of liver fibrosis.