论文部分内容阅读
目的:观察荔枝核总黄酮(total flavone from Litchi chinensis Sonn,TFL)对二甲基亚硝胺(DMN)诱导的肝纤维化大鼠肝脏组织转移生长因子-β1(TGF-β1)/Smad信号通路中关键信号传导分子TGF-β1,Smad3,Smad7表达水平的变化,探讨TFL抗纤维化的作用机制。方法:SD大鼠ip DMN 4周建立大鼠肝纤维化模型,以ig水飞蓟宾为阳性对照50 mg·kg-1组,用不同剂量的TFL(400,200,100 mg·kg-1·d-1)ig给药,造模当日开始分组给药,每日1次,共给药6周。于实验第6周末处死大鼠,抽取下腔静脉血检测天冬氨酸转氨酶(AST),丙氨酸转氨酶(ALT),留取肝脏同一部位行HE,Masson染色观察大鼠病理改变及肝纤维化程度,采用RT-PCR法检测TGF-β1,Smad3,Smad7 mRNA的表达。结果:与空白对照组比较,模型组大鼠的肝纤维化程度明显增加,血清AST,ALT均显著升高,肝组织TGF-β1,Smad3 mRNA的表达明显增强(P<0.05),Smad7 mRNA的表达显著减弱(P<0.05);与模型组比较,TFL各剂量组和水飞蓟宾组血清AST,ALT均明显低于模型组,肝脏TGF-β1,smad3的表达明显降低(P<0.05),而smad7则有所升高。结论:荔枝核总黄酮可减轻实验性大鼠肝损伤及改善肝纤维化程度,其作用机制可能与抑制TGF-β1,Smad3 mRNA的表达,上调Smad7 mRNA的表达有密切关系。
OBJECTIVE: To observe the effect of total flavone from Litchi chinensis Sonn (TFL) on the expression of TGF-β1 / Smad in hepatic fibrosis rats induced by dimethylnitrosamine (DMN) In the key signal transduction molecules TGF-β1, Smad3, Smad7 expression levels, to explore the anti-fibrosis mechanism of TFL. Methods: The rat model of hepatic fibrosis was established by intraperitoneal injection of ip DMN for 4 weeks in SD rats. The serum silybin was used as a positive control (50 mg · kg -1) and the TFL (400,200,100 mg · kg -1 · d -1) ) ig administration, the day of modeling began to group administration, 1 day, a total of 6 weeks. At the end of the experiment, rats were sacrificed at the end of 6th week. The aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were extracted from inferior vena cava and the same part of the liver was taken for HE and Masson staining to observe the pathological changes of rat and liver fibrosis The expression of TGF-β1, Smad3 and Smad7 mRNA was detected by RT-PCR. Results: Compared with the blank control group, the levels of hepatic fibrosis, serum AST and ALT in the model group were significantly increased, the expression of TGF-β1 and Smad3 mRNA in the liver tissue were significantly increased (P <0.05), the expression of Smad7 mRNA (P <0.05). Compared with the model group, the levels of AST and ALT in each dose group and silybin group were significantly lower than those in model group, and the expressions of TGF-β1 and smad3 in liver tissue were significantly decreased (P <0.05) , While smad7 increased. Conclusion: The total flavonoids of litchi nucleus can reduce liver injury and improve the degree of hepatic fibrosis in experimental rats. The mechanism may be related to inhibiting the expression of TGF-β1 and Smad3 mRNA and up-regulating the expression of Smad7 mRNA.