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目的:研究蚯蚓提取物“地龙2号”对肝纤维化模型大鼠肝组织α-平滑肌肌动蛋白(α-SMA)及转化生长因子-β1(TGF-β1)蛋白表达水平的影响。方法:雄性Wistar大鼠随机分成6组:模型组,CCl4造模同时仅用单蒸水10ml·kg-1·d-1灌胃;地龙2号大剂量组,造模同时用地龙2号50ml·kg-1·d-1灌胃;地龙2号小剂量组,造模同时用地龙2号25ml·kg-1·d-1灌胃;阳性对照组,造模同时用秋水仙碱0郾1ml·kg-1·d-1灌胃;阴性对照组,皮下注射与造模同剂量的不含CCl4的花生油,不用药物干预;正常组,不注射CCl4、花生油,也不用任何药物干预。8周后处死大鼠,分别应用HE染色观察大鼠肝脏组织的病理改变,并用免疫组织化学染色法检测肝组织中α-SMA及TGF-β1蛋白的表达情况。结果:地龙2号大、小剂量组肝纤维化的程度均明显减轻,α-SMA、TGF-β1蛋白表达均显著降低,而秋水仙碱组无显著变化。各实验组肝纤维化程度与α-SMA、TGF-β1蛋白的表达水平均呈明显的正相关。结论:地龙2号具有抗实验性大鼠肝纤维化作用,其机理可能与其抑制肝星状细胞活化及TGF-β1蛋白表达有关。
OBJECTIVE: To study the effect of extract “Dilong 2” on hepatic tissue expression of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in rat liver fibrosis model. METHODS: Male Wistar rats were randomly divided into 6 groups: model group, CCl4 was intragastrically administered with only 10ml·kg-1·d-1 of distilled water, and Dilong 2 high-dose group was used. 50ml·kg-1·d-1 gavage; Xiaolong No.2 low-dose group, at the same time with modeling Dilong 2 No. 25ml·kg-1·d-1 gavage; Positive control group, modeling with colchicine simultaneously 0 郾1 ml·kg-1·d-1 gavage; negative control group, subcutaneous injection and modeling the same dose of peanut oil without CCl4 without drug intervention; normal group, without injection of CCl4, peanut oil, without any drug intervention . Eight weeks later, rats were sacrificed and HE staining was used to observe the pathological changes of liver tissue. The expression of α-SMA and TGF-β1 protein in liver tissue was detected by immunohistochemical staining. Results: The degree of hepatic fibrosis in the large and small doses of Dilong 2 was significantly reduced, and the expression of α-SMA and TGF-β1 protein were significantly decreased, while there was no significant change in the colchicine group. The degree of hepatic fibrosis in each experimental group was positively correlated with the expression levels of α-SMA and TGF-β1 protein. Conclusion: Dilong 2 has anti-fibrotic effect in experimental rats, and its mechanism may be related to the inhibition of hepatic stellate cell activation and TGF-β1 protein expression.