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目的观察酒精性肝纤维化与盘状结构域受体2(DDR2)的关系以及复方甘草酸苷(GGT)治疗对二者的影响。方法48只大鼠随机分为正常对照组、模型组、停酒组、未停酒组、停酒治疗组及未停酒治疗组(n=8)。模型组酒精灌胃16周后,与正常对照组一起处死。其余4组于酒精灌胃16周后分别予以停酒、不停酒、停酒+GGT治疗、不停酒+GGT治疗4周,至20周末全部处死。检测各组血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PCⅢ)及Ⅳ型胶原(CⅣ)含量,取肝组织进行HE染色及Masson染色观察其组织病理学变化,实时荧光定量PCR和Western blot蛋白印迹法分别检测肝组织DDR2 mRNA和蛋白表达。结果酒精灌胃16周后,大鼠肝组织呈明显肝纤维化病理表现,血清HA、LN、PCⅢ、CⅣ水平和肝组织胶原面密度及DDR2表达均较正常对照组升高(P<0.01)。停酒治疗组与停酒未治疗组、未停酒治疗组与未停酒未治疗组比较,上述各指标均降低(P<0.05)。结论CGT对酒精性肝纤维化具有一定的治疗作用,其作用可能与下调DDR2的表达相关。
Objective To investigate the relationship between alcoholic liver fibrosis and disk-shaped domain receptor 2 (DDR2) and the effect of compound glycyrrhizin (GGT) treatment on both. Methods Forty - eight rats were randomly divided into normal control group, model group, stop alcohol group, non - stop alcohol group, stop alcohol treatment group and untreated alcohol group (n = 8). After 16 weeks, the model group rats were sacrificed along with the normal control group. The remaining 4 groups were stopped alcohol after 16 weeks of gastric perfusion, stop alcohol, stop alcohol + GGT treatment, non-stop alcohol + GGT treatment for 4 weeks to 20 weeks were all executed. The content of HA, LN, PCⅢ and CⅣ in serum of each group were detected. The histopathological changes of liver tissues were observed by HE staining and Masson staining, Real-time fluorescence quantitative PCR and Western blot were used to detect the expression of DDR2 mRNA and protein in liver tissue. Results After 16 weeks of alcohol administration, the pathological changes of hepatic fibrosis were observed in liver tissue of rats. The levels of serum HA, LN, PCⅢ and CⅣ, the collagen surface density and the expression of DDR2 in liver tissue were higher than those in normal control group (P <0.01) . All of the above parameters were lower in the alcohol-withdrawal group and those in the untreated alcohol group, the non-alcohol-treated group, and the untreated alcohol-treated group (P <0.05). Conclusions CGT has a certain therapeutic effect on alcoholic liver fibrosis, and its effect may be related to the down-regulation of the expression of DDR2.