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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 H_2O(1 cmH_2O= 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。
Objective To observe the angiogenic effect of hVEGF-D in portal vein of rats with biliary cirrhosis and its effect on hepatic fibrosis and portal pressure. Methods Thirty (30) SD rats were subjected to common bile duct ligation to establish a model of biliary cirrhosis. The rats in the treatment group were injected with PCHO / hVEGF-D 150 μg / g twice a day for two weeks. The degree of hepatic fibrosis was compared between two groups (hematoxylin-eosin staining, Law), portal pressure, VEGF protein expression, changes in hepatic microvessel density. Results The degree of liver fibrosis was significantly lower than that before injection. The portal venous pressure was (15.45 ± 1.97) cm H 2 O (1 cmH 2 O = 0.098 kPa) before treatment and (12.56 ± 1. 86), the difference was statistically significant (P <0.05). The average staining score of VEGF protein expression in the treatment group was 6.56 ± 1.81, and the control group was 4.4 ± 1.02, the difference was statistically significant (P <0.01). Vascular count in the treatment group was 14.33 ± 3.24; cirrhosis control was 9.2 ± 1.48 (P <0.01). Conclusion The portal vein injection of vascular endothelial growth factor D expression vector in portal vein of rats with biliary cirrhosis can promote the formation of intrahepatic vessels to a certain degree, reduce the degree of hepatic fibrosis and decrease the portal vein pressure.