【摘要】 目的观察胆汁性肝硬变大鼠门静脉注射血管内皮生长因子D（hVEGF-D）后的促血管形成效应以及对肝纤维化和门静脉压力的影响。方法30只SD大鼠胆总管结扎法制作胆汁性肝硬变模型,治疗组门静脉注射PCHO／hVEGF-D 150μg／只,2周后比较肝组织纤维化程度（苏木素-伊红染色、浸银染色法）、门静脉压力、VEGF蛋白质表达、肝组织微血管密度改变。结果肝组织纤维化程度较注射前明显降低;门静脉压力治疗前为（15．45±1．97）cm H₂O（1 cmH₂O= 0．098 kPa）;治疗后则变为（12．56±1．86）,差异有统计学意义（P<0．05）。治疗组VEGF蛋白质表达平均染色积分为6．56±1．81,肝硬变对照组4．4±1．02,差异有统计学意义（P<0．01）。治疗组血管计数为14．33±3．24;肝硬变对照为9．2±1．48（P<0．01）。结论胆汁性肝硬变大鼠门静脉注射血管内皮生长因子D表达载体后可以一定程度上促进肝内血管形成、减缓肝纤维化程度降低门静脉压力。更多还原

【Abstract】 To investigate the expression efficiency and its therapeutic value of plasmid vector encoding for vascular endothelial growth factor D （PCHO/hVEGF-D） after intravenous injection to cirrhotic rat liver due to cholestasis. Methods The model of biliary cirrhosis was established in 30 rats by ligation of common bile duct for 4 weeks. The pressure of portal vein, fibrosis change in liver, VEGF protein expression and vascular density were compared before and 2 weeks after administration of PCHO/ hVEGF-D 150 mg for each. VEGF protein was identified by histoimmunochemistry and vascular endothelial cells were marked with Factor Ⅷ. Results The average pressure of portal vein before treatment was 15.45± 1.97 cm H₂O, and decreased to 12.56±1.86 with significant difference after treatment with PCHO/hVEGF-D （P<0.05）. The fibrosis degree was also relieved remarkably. The VEGF protein expression was elevated to 6.56 + 1.81 while only 4.4 ± 1.02 in control group （P < 0.01）. The average number of capillaries was statistically more in treatment group than in control group （14.33± 3.24 vs 9.2±1.48,P<0.01）.Conclusion Venous injection with PCHO/HVEGF-D to rat could induce angio-genesis as a result of high expression of VEGF. Liver fibrosis and portal pressure could be relieved after angiogenesis in cirrhotic rats due to cholestasis.更多还原