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目的:从整体水平研究复方桃红四物汤对四氯化碳所致肝纤维化模型小鼠肝组织血管内皮生长因子(VEGF)、含激酶插入区受体(KDR)及Flt-1蛋白与mRNA表达的影响。方法:昆明小鼠60只,随机分组为空白组,模型组,秋水仙碱组,桃红四物汤高、中、低(17.00、8.50、4.25g/kg)剂量组,采用左侧腹股沟处皮下注射四氯化碳花生油溶液建立小鼠肝纤维化模型,给药6周后,运用酶联免疫吸附测定(ELISA)法检测肝组织VEGF蛋白含量;蛋白印迹法(Western blot)测定小鼠肝脏KDR、Flt-1蛋白的表达;逆转录PCR(RT-PCR)法测定小鼠肝脏VEGF、KDR及Flt-1 mRNA表达。结果:桃红四物汤治疗后,桃红四物汤高、中剂量组肝组织VEGF蛋白表达量较模型组降低(P<0.05,P<0.01),中药高剂量组肝组织KDR与Flt-1蛋白表达较模型组显著降低(P<0.05);而桃红四物汤高、中剂量组肝组织VEGF、KDR与Flt-1 mRNA表达较模型组、秋水仙碱组明显减少(P<0.01),并且呈现一定的量效正相关。结论:桃红四物汤能够降低肝纤维化病理血管生成相关因子的表达,减缓病理性的微血管生成可能是其改善肝纤维化的机制之一。
OBJECTIVE: To study the effects of compound Taohongsiwu Decoction (MCHH) on the levels of vascular endothelial growth factor (VEGF), KDR-containing kinase and Flt-1 protein and mRNA in hepatic tissue of liver fibrosis induced by carbon tetrachloride The impact of expression. Methods: Sixty Kunming mice were randomly divided into blank group, model group, colchicine group and Taohong Siwu Tang high, medium and low dose groups (17.00, 8.50, 4.25g / kg) The liver fibrosis model was established by injecting carbon tetrachloride peanut oil solution. After 6 weeks of administration, the VEGF protein content in liver tissue was detected by enzyme-linked immunosorbent assay (ELISA); Western blot was used to detect the KDR , Flt-1 protein expression; reverse transcription PCR (RT-PCR) method for the determination of liver VEGF, KDR and Flt-1 mRNA expression. Results: After treated with Taohong Siwu Decoction, the expression of VEGF protein in liver tissue of high and medium dose Taohong Siwu Decoction group was lower than that of model group (P <0.05, P <0.01). KDR and Flt-1 protein The expressions of VEGF, KDR and Flt-1 mRNA in liver tissue of high and middle dose of Taohong Siwu decoction group were significantly lower than those in model group and colchicine group (P <0.01), and Showing a certain amount of effective positive correlation. Conclusion: Taohong Siwu decoction can reduce the expression of pathological angiogenesis-related factors in liver fibrosis, and alleviate pathological microangiogenesis may be one of the mechanisms of improving hepatic fibrosis.