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血管内皮生长因子D基因转移对胆汁性肝硬变大鼠肝纤维化和门静脉压力的影响

The effect on liver fibrosis and portal pressure after administration of expression vector encoding for endothelial growth factor D in biliary cirrhotic rats

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【作者】 施宝民杨镇王秀艳徐健穆庆岭吴泰璜

【Author】 SHI Bao-min , YANG Zhen, WANG Xiu-yan, et al. Department of General Surgery, Shandong Provincial Hospital, Jinan 250021, China

【机构】 山东省立医院普外科华中科技大学同济医学院附属同济医院外科山东省立医院超声诊疗中心山东省立医院普外科

【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。

【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.

【基金】 国家自然科学基金资助项目(30300341)山东省优秀中青年科学家奖励基金资助项日(O1BS57)
  • 【文献出处】 中华实验外科杂志 ,Chinese Journal of Experimental Surgery , 编辑部邮箱 ,2006年03期
  • 【分类号】R575.2
  • 【被引频次】3
  • 【下载频次】66
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