核因子—κBp65对肝门静脉海绵样变性大鼠门静脉及其周围组织中血管内皮生长因子、肿瘤坏死因子—α、内皮素表达的影响

梁杰聪　温哲　宋俏莉

[摘要] 目的 探讨核因子-κB（NF-κB）p65对肝门静脉海绵样变性（CTPV）大鼠门静脉及其周围组织中血管内皮生长因子（VEGF）、肿瘤坏死因子-α（TNF-α）、内皮素（ET-1）表达的影响。 方法 将124只雄性SD大鼠按照随机数字表法分为对照组31只，假手术组31只，CTPV组31只，NF-κB p65抑制组31只。CTPV组与NF-κB p65抑制组实施CTPV造模处理。对照组、假手术组及CTPV组每日于皮内注射0.9%氯化钠注射液0.2 mL，而NF-κB p65抑制组每日于皮内注射100 mg/kg的吡咯烷二硫代氨基甲酸盐，持续注射1个月。停药0.5个月后，对门静脉、周围组织中VEGF、TNF-α、ET-1表达情况进行检测。 结果 对照组与假手术组门静脉压比较，差异无统计学意义（P > 0.05）。CTPV组及NF-κB p65抑制组的门静脉压高于对照组，差异均有统计学意义（均P < 0.05）。NF-κB p65抑制组的门静脉压低于CTPV组，差异有统计学意义（P < 0.05）。对照组与假手术组的VEGF与ET-1含量相比，差异无统计学意义（P > 0.05）。CTPV组及NF-κB p65抑制组的VEGF与ET-1含量高于对照组，差异均有统计学意义（均P < 0.05）。NF-κB p65抑制组的VEGF、TNF-α与ET-1含量低于CTPV组，差异均有统计学意义（均P < 0.05）。对照组和假手术组NF-κB p65含量比较，差异无统计学意义（P > 0.05）。CTPV组及NF-κB p65抑制组的NF-κB p65含量高于对照组，且NF-κB p65抑制组的NF-κB p65含量低于CTPV组，差异均有统计学意义（均P < 0.05）。经Spearman相关性分析，NF-κB p65与VEGF、TNF-α及ET-1表达均呈正相关（r = 0.620、0.637、0.630，均P < 0.05）。 结论 VEGF、TNF-α、ET-1及NF-κB p65均参与CTPV的发生及发展，且NF-κB p65对VEGF、TNF-α、ET-1具有调控作用，NF-κB p65与VEGF、TNF-α、ET-1表达呈正相关。

[关键词] 核因子-κB；肝门静脉海绵样变性；大鼠门静脉；血管内皮生长因子；肿瘤坏死因子-α；内皮素

[中图分类号] R-332 [文献标识码] A [文章编号] 1673-7210（2015）09（c）-0018-04

[Abstract] Objective To explore influence of NF-κB p65 on vascular endothelial growth factor （VEGF）， tumor necrosis factor-α （TNF-α）， endothelin （ET-1） expression in portal vein and its surrounding tissue of rat with cavernous transformation of portal vein （CTPV）. Methods 124 male SD rats were divided into control group with 31 cases， sham operation group with 31 cases， CTPV group with 31 cases and NF-κB p65 inhibit group with 31 cases according to random digital table method. CTPV model processing was implemented in CTPV group and NF-κB p65 inhibit group. Control group， sham operation group and CTPV group daily to intradermal injection of 0.2 mL of 0.9% Sodium Chloride Injection， while NF-κB p65 inhibit group daily to intradermal injection of 100 mg/kg of PDTC， continuous injection of a month. After drug withdrawal of half a month， VEGF， TNF-α， ET-1 expression in portal vein and its surrounding tissue were detected. Results PVP of control group and sham operation group had no statistical difference （P > 0.05）. PVP of CTPV group and NF-κB p65 inhibit group were higher than those of control group， differences were statistically significant （all P < 0.05）. PVP of NF-κB p65 inhibit group was lower than that of CTPV group， with statistical difference （P < 0.05）. VEGF， ET-1 content of control group and sham operation group were compared， with no statistical differences （P > 0.05）. VEGF， ET-1 content of CTPV group and NF-κB p65 inhibit group were higher than those of control group， differences were statistically significant （all P < 0.05）. VEGF， TNF-α， ET-1 content of NF-κB p65 inhibit group were lower than those of CTPV group， with statistical differences （all P < 0.05）. NF-κB p65 content of control group and sham operation group had no statistical difference （P > 0.05）. NF-κB p65 content of CTPV group and NF-κB p65 inhibit group were higher than those of control group， NF-κB p65 content of NF-κB p65 inhibit group was lower than that of CTPV group， with statistical differences （all P < 0.05）. Spearman correlation analysis showed， NF-κB p65 and VEGF， TNF-α， ET-1 expression were positively correlated （r = 0.620， 0.637， 0.630，all P < 0.05）. Conclusion VEGF， TNF-α， ET-1 and NF-κB p65 are all involved in the occurrence and development of CTPV. NF-κB p65 has a regulatory effect on VEGF， TNF-α and ET-1. NF-κB p65 is positively correlated with the expression of VEGF， TNF-α and ET-1.