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[目的]研究银杏叶提取物(EGb)对肝纤维化大鼠的保护作用及其可能机制。[方法]36只Wistar大鼠随机分为空白对照组、模型组、EGb预防4、8周组。用CCl4腹腔注射诱导大鼠肝纤维化模型,采用免疫组化半定量法观察EGb干预4、8周后肝组织转化生长因子β1(TGF-β1)I、型胶原(Col I)蛋白的表达,苏木精-伊红及苦味酸-酸性品红胶原染色法观察肝组织病理形态学的改变,并检测肝功能、脂质过氧化指标等。[结果]与模型组相比,EGb干预治疗4、8周后,大鼠肝组织TGF-β1、Col I蛋白的表达显著降低(P<0.05),并显著改善肝纤维化分级(P<0.05),使血清丙氨酸氨基转移酶、天冬氨酸转氨酶降低,清蛋白升高(P<0.01),并使肝组织丙二醛明显降低(P<0.01),8周较4周更明显。[结论]EGb具有抗脂质过氧化,降低TGF-β1的表达、抑制Col I合成的作用。
[Objective] To study the protective effect of Ginkgo biloba extract (EGb) on hepatic fibrosis in rats and its possible mechanism. [Methods] Thirty-six Wistar rats were randomly divided into blank control group, model group and EGb prevention group for 4 and 8 weeks. The hepatic fibrosis model induced by intraperitoneal injection of CCl4 was used to observe the expression of transforming growth factor-β1 (TGF-β1) I and collagen I (Col I) protein in liver tissue after 4 and 8 weeks of intervention with EGb. Hematoxylin-eosin and picric acid-acid fuchsin collagen staining was used to observe the pathological changes of liver tissue, and liver function, lipid peroxidation, etc. were detected. [Results] Compared with the model group, the expression of TGF-β1 and Col I protein in the rat liver tissue was significantly decreased after 4 and 8 weeks of intervention (P<0.05), and the liver fibrosis grade was significantly improved (P<0.05). ), serum alanine aminotransferase, aspartate aminotransferase decreased, albumin increased (P <0.01), and liver tissue malondialdehyde decreased significantly (P <0.01), 8 weeks more obvious than 4 weeks . [Conclusion] EGb has anti-lipid peroxidation, reduced TGF-β1 expression and inhibited Col I synthesis.