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目的:以二甲基亚硝胺(DMN)诱导的大鼠肝纤维化为模型,研究狗肝菜多糖对DMN诱导的肝纤维化大鼠TGF-β1/Smads信号通路的影响。方法:将96只大鼠随机分为对照组、模型组、狗肝菜多糖(300 mg/kg,200 mg/kg,100 mg/kg)组和秋水仙碱组(0.12 mg/kg)。除对照组以外,其余各组大鼠均腹腔注射0.5%DMN溶液(1.5 ml/kg),隔天1次,在首次注射DMN同时,各组大鼠灌胃给予相应的药物,而正常组和模型组灌胃给予相应体积的生理盐水溶液,每天给药1次,连续5周,5周末眼球取血,脱臼致死,收取肝脏。生化法检测血清中碱性磷酸酶(ALP)、谷氨酰氨基转移酶(GGT)水平;酶联免疫法检测(ELISA)血清中透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原(PCⅢ)和Ⅳ型胶原(Ⅳ-C)含量。苏木精-伊红染色(HE染色)进行肝组织病理学检查;蛋白质印迹法(Western blot)检测肝组织a-平滑肌肌动蛋白(a-SMA)、转化生长因子β1(TGF-β1)和Smad2/3/7的蛋白表达情况。结果:与模型组比较,经狗肝菜多糖(300 mg/kg,200 mg/kg,100 mg/kg)组干预后,血清中ALP、GGT、HA、LN、PCⅢ和Ⅳ-C水平显著降低;肝组织中a-SMA、TGF-β1、Smad2/3的蛋白表达被抑制,而Smad7的表达得到促进;病理切片显示肝纤维化大鼠肝组织炎症坏死程度和肝纤维化病变程度较模型组明显减轻。结论:狗肝菜多糖具有抗DMN诱导的大鼠肝纤维化的作用,其机制与TGF-β1/Smads信号通路相关因子的表达有关。
OBJECTIVE: To investigate the effect of Hepaticus chinensis polysaccharides on TGF-β1 / Smads signaling in DMN-induced hepatic fibrosis in rats induced by dimethylnitrosamine (DMN). Methods: Ninety-six rats were randomly divided into control group, model group, Hepatic polyglucose (300 mg / kg, 200 mg / kg, 100 mg / kg) group and colchicine group (0.12 mg / kg) Rats in each group were given intraperitoneal injection of 0.5% DMN solution (1.5 ml / kg) except for the control group, and once a day after the first injection of DMN. At the same time, the rats in each group were given gavage with corresponding drugs, The model group was given the corresponding volume of saline solution by gavage. The medicine was administered once a day for 5 consecutive weeks and the eyeballs were taken blood and dislocated 5 weeks later to collect the liver. Serum levels of ALP and GGT were detected by biochemical methods. Hyaluronic acid (HA), laminin (LN), serum nitric oxide synthase Type procollagen (PC Ⅲ) and type Ⅳ collagen (Ⅳ-C) content. Hematoxylin-eosin staining (HE staining) was used for histopathological examination of liver tissue. Western blotting was used to detect a-SMA, TGF-β1 and Smad2 / 3/7 protein expression. Results: Compared with the model group, the levels of ALP, GGT, HA, LN, PCⅢ and Ⅳ-C in the serum of the model group were significantly decreased after intervention with 300 mg / kg, 200 mg / kg and 100 mg / The protein expression of a-SMA, TGF-β1 and Smad2 / 3 was inhibited in the tissue and the expression of Smad7 was promoted. Pathological examination showed that the degree of inflammation, necrosis and hepatic fibrosis in liver fibrosis rats were significantly reduced compared with the model group . CONCLUSION: The Hepatic Giraldo polysaccharide has anti-DMN-induced hepatic fibrosis in rats. The mechanism is related to the expression of TGF-β1 / Smads signal pathway related factors.