摘要
目的探讨积雪草苷(asiaticoside,AS)对乙型肝炎模型大鼠肝纤维化及转化生长因子-β1(transforming growth factor-β1,TGF-β1)/Smad信号通路的影响。方法将造模成功的48只SD大鼠随机分为模型(Model)组、AS组(50 mg/kg)、Smad激活剂SRI-011381组(30 mg/kg Smad激活剂SRI-011381)、AS+SRI-011381组(50 mg/kg AS+30mg/kg SRI-011381),另取12只健康大鼠为健康对照(normal control,NC)组,检测其AST、ALT、透明质酸(hyaluronic acid,HA)、层粘蛋白(laminin,LN)、Ⅲ型前胶原(procollagen type Ⅲ,PCⅢ)、HBsAg、HBeAg水平,肝组织形态及纤维化程度以及、肝组织TGF-β1/Smad通路信号蛋白表达。结果NC组肝组织形态正常、无纤维增生;Model组肝组织坏死、水肿、细胞排列紊乱、纤维结缔组织增生。与Model组相比,AS组肝病变减轻。SRI-011381组肝病变最重。AS+SRI-011381组肝损伤和纤维化程度较AS组加重。与NC组相比,Model组ALT、AST、HBsAg、HBeAg、HA、LN和PCⅢ水平及TGF-β1、p-Smad2/Smad2、p-Smad1/5/9/Smad1/5/9蛋白水平均显著升高(P均<0.05);与Model组比较,AS组ALT、AST、HBsAg、HBeAg、HA、LN和PCⅢ水平及TGF-β1、p-Smad2/Smad2、p-Smad1/5/9/Smad1/5/9蛋白水平均显著下降(P均<0.05);而SRI-011381组呈现相反的趋势(P均<0.05)。与AS组相比,AS+SRI-011381组ALT、AST、HBsAg、HBeAg、HA、LN、PCⅢ水平及TGF-β1、p-Smad2/Smad2、p-Smad1/5/9/Smad1/5/9蛋白水平均显著升高(P均<0.05)。结论AS可能通过抑制TGF-β1/Smad通路信号改善乙型肝炎大鼠的肝纤维化程度。
Objective To investigate the influences of asiaticoside(AS)on liver fibrosis and transforming growth factor-β1(TGF-β1)/Smad signaling pathway in hepatitis B model rats.Method Fourty-eight SD rats were randomly grouped into control group(NC)group,Model group,AS group(50 mg/kg),Smad activator SRI-011381 group(30 mg/kg Smad activator SRI-011381),and AS+SRI-011381group(50 mg/kg AS+30 mg/kg SRI-011381).Twelve healthy rats were taken as normal control(NC)group.The contents of serum aspartate aminotransferase(AST),alanine aminotransferase(ALT),hyaluronic acid(HA),laminin(LN),procollagen type Ⅲ(PCⅢ),adventitia Protein(HBs Ag),nucleocapsid protein(HBeAg),the liver tissue morphology and fibrosis,and the expression of TGF-β1/Smad pathway proteins in liver tissue were detected.Results Compared with the NC group,the liver tissue had normal morphology and no fibrosis,while the Model group had liver tissue necrosis,edema,disordered cell arrangement,and fibrous connective tissue hyperplasia.Compared with the Model group,the liver lesions in AS group were alleviated.SRI-011381 group had the most severe liver disease.The liver injury and fibrosis in AS+SRI-011381 group were more severe than those in AS group.Compared with the NC group,the levels of ALT,AST,HBsAg,HBeAg,HA,LN and PCⅢ and the protein levels of TGF-β1,p-Smad2/Smad2,p-Smad1/5/9/Smad1/5/9 in the Model group were obviously increased(P<0.05);compared with the Model group,the levels of ALT,AST,HBsAg,HBeAg,HA,LN and PCⅢ and the protein levels of TGF-β1,p-Smad2/Smad2,p-Smad1/5/9/Smad1/5/9 in the AS group were obviously decreased(P<0.05);the SRI-011381group showed the opposite trend(P<0.05).Compared with AS group,the levels of ALT,AST,HBsAg,HBeAg,HA,LN and PCⅢ and the protein levels of TGF-β1,p-Smad2/Smad2,p-Smad1/5/9/Smad1/5/9 in the AS+SRI-011381 group wereobviously increased(P<0.05).Conclusions AS may improve liver fibrosis in hepatitis B rats by inhibiting TGF-β1/Smad pathway.
作者
汪燕
王立志
王运东
孟冈
高冕
孙文锦
WANG Yan;WANG Li-zhi;WANG Yun-dong;MENG Gang;GAO Mian;SUN Wen-jin(Infection Department,Ezhou Central Hospital,436000,China)
出处
《传染病信息》
2022年第6期496-501,共6页
Infectious Disease Information
