Objective: To elucidate the protective effect of Gan Shen Fu Fang(GSFF) on liver endothelial cells in common bile duct-ligated(CBDL) rats.Materials and Methods: Cirrhosis was induced by common bile duct ligation. The ...Objective: To elucidate the protective effect of Gan Shen Fu Fang(GSFF) on liver endothelial cells in common bile duct-ligated(CBDL) rats.Materials and Methods: Cirrhosis was induced by common bile duct ligation. The rats were divided into three groups: sham group, CBDL group, and GSFF group. After 2 weeks of ligation, rats in the GSFF group were administered GSFF. After 4 weeks, the hydroxyproline(Hyp)content of liver tissues was spectrophotometrically determined. The histological changes were evaluated by H and E and Masson staining.Transmission electron microscopy(TEM) and scanning electron microscopy(SEM) were used to observe the ultrastructural changes in the liver, especially in the liver sinusoidal endothelial cells(LSECs). Results: Hyp synthesis was significantly inhibited by GSFF, which agreed with the results from H and E and Masson staining for liver fibrosis. The TEM observations of CBDL rats revealed reduced hepatocyte microvilli and deposited fibrous tissue underneath LSECs. SEM confirmed the TEM findings and showed that the fenestrae of LSECs decreased and even disappeared in CBDL rats. The morphological results indicated hepatic sinusoid capillarization. GSFF promoted the restoration of fenestrae and reversed hepatic sinusoid capillarization. Conclusion: GSFF can inhibit Hyp synthesis, restore the fenestrae of LSECs, and reverse hepatic sinusoid capillarization in CBDL rats. These results provide a basis for future detailed investigations of the mechanism of action of GSFF in LSECs.展开更多
目的:研究JNK和MMP-2、TIMP-2在肝脏纤维化大鼠模型中的表达以及中药复方制剂肝复康对肝脏纤维化的治疗作用及其机制。方法:大鼠肝脏纤维化模型采用CCl4作用12周(0.5mg/kg,2次/周);治疗组大鼠在CCl4作用同时从第9周开始,给予肝复康(31.2...目的:研究JNK和MMP-2、TIMP-2在肝脏纤维化大鼠模型中的表达以及中药复方制剂肝复康对肝脏纤维化的治疗作用及其机制。方法:大鼠肝脏纤维化模型采用CCl4作用12周(0.5mg/kg,2次/周);治疗组大鼠在CCl4作用同时从第9周开始,给予肝复康(31.25,312.5 and 3125mg/kg/d,po);设立正常对照组;所有大鼠于20周末处死;HE染色光镜观察肾脏病理改变,并进行组织学评分;RT-PCR检测肝组织JNK和MMP-2、TIMP-2mRNA水平。对三者的mRNA水平进行相关性分析。结果:HE染色观察到显著肝脏纤维化改变,肝脏纤维化模型复制成功;模型组JNK和MMP-2、TIMP-2基因表达较正常对照组明显增加(P<0.01);三者的mRNA水平在各组间均呈显著正相关;GFK中剂量治疗组二者表达显著降低。结论:GFK可以通过抑制JNK和MMP-2、TIMP-2的mRNA表达,发挥抗纤维化的作用。展开更多
基金supported by the Beijing Municipal Natural Science Foundation[7144223]supported by the China Scholarship Council program(201606555017)the Research Program of Beijing University of Chinese Medicine(2017-JYB-JS)
文摘Objective: To elucidate the protective effect of Gan Shen Fu Fang(GSFF) on liver endothelial cells in common bile duct-ligated(CBDL) rats.Materials and Methods: Cirrhosis was induced by common bile duct ligation. The rats were divided into three groups: sham group, CBDL group, and GSFF group. After 2 weeks of ligation, rats in the GSFF group were administered GSFF. After 4 weeks, the hydroxyproline(Hyp)content of liver tissues was spectrophotometrically determined. The histological changes were evaluated by H and E and Masson staining.Transmission electron microscopy(TEM) and scanning electron microscopy(SEM) were used to observe the ultrastructural changes in the liver, especially in the liver sinusoidal endothelial cells(LSECs). Results: Hyp synthesis was significantly inhibited by GSFF, which agreed with the results from H and E and Masson staining for liver fibrosis. The TEM observations of CBDL rats revealed reduced hepatocyte microvilli and deposited fibrous tissue underneath LSECs. SEM confirmed the TEM findings and showed that the fenestrae of LSECs decreased and even disappeared in CBDL rats. The morphological results indicated hepatic sinusoid capillarization. GSFF promoted the restoration of fenestrae and reversed hepatic sinusoid capillarization. Conclusion: GSFF can inhibit Hyp synthesis, restore the fenestrae of LSECs, and reverse hepatic sinusoid capillarization in CBDL rats. These results provide a basis for future detailed investigations of the mechanism of action of GSFF in LSECs.
文摘目的:研究JNK和MMP-2、TIMP-2在肝脏纤维化大鼠模型中的表达以及中药复方制剂肝复康对肝脏纤维化的治疗作用及其机制。方法:大鼠肝脏纤维化模型采用CCl4作用12周(0.5mg/kg,2次/周);治疗组大鼠在CCl4作用同时从第9周开始,给予肝复康(31.25,312.5 and 3125mg/kg/d,po);设立正常对照组;所有大鼠于20周末处死;HE染色光镜观察肾脏病理改变,并进行组织学评分;RT-PCR检测肝组织JNK和MMP-2、TIMP-2mRNA水平。对三者的mRNA水平进行相关性分析。结果:HE染色观察到显著肝脏纤维化改变,肝脏纤维化模型复制成功;模型组JNK和MMP-2、TIMP-2基因表达较正常对照组明显增加(P<0.01);三者的mRNA水平在各组间均呈显著正相关;GFK中剂量治疗组二者表达显著降低。结论:GFK可以通过抑制JNK和MMP-2、TIMP-2的mRNA表达,发挥抗纤维化的作用。
