核因子—κBp65對肝門靜脈海綿樣變性大鼠門靜脈及其周圍組織中血管內皮生長因子、腫瘤壞死因子—α、內皮素表達的影響

梁杰聰　溫哲　宋俏莉

[摘要] 目的 探討核因子-κB（NF-κB）p65對肝門靜脈海綿樣變性（CTPV）大鼠門靜脈及其周圍組織中血管內皮生長因子（VEGF）、腫瘤壞死因子-α（TNF-α）、內皮素（ET-1）表達的影響。 方法 將124只雄性SD大鼠按照隨機數字表法分為對照組31只，假手術組31只，CTPV組31只，NF-κB p65抑制組31只。CTPV組與NF-κB p65抑制組實施CTPV造模處理。對照組、假手術組及CTPV組每日于皮內注射0.9%氯化鈉注射液0.2 mL，而NF-κB p65抑制組每日于皮內注射100 mg/kg的吡咯烷二硫代氨基甲酸鹽，持續注射1個月。停藥0.5個月后，對門靜脈、周圍組織中VEGF、TNF-α、ET-1表達情況進行檢測。 結果 對照組與假手術組門靜脈壓比較，差異無統計學意義（P > 0.05）。CTPV組及NF-κB p65抑制組的門靜脈壓高于對照組，差異均有統計學意義（均P < 0.05）。NF-κB p65抑制組的門靜脈壓低于CTPV組，差異有統計學意義（P < 0.05）。對照組與假手術組的VEGF與ET-1含量相比，差異無統計學意義（P > 0.05）。CTPV組及NF-κB p65抑制組的VEGF與ET-1含量高于對照組，差異均有統計學意義（均P < 0.05）。NF-κB p65抑制組的VEGF、TNF-α與ET-1含量低于CTPV組，差異均有統計學意義（均P < 0.05）。對照組和假手術組NF-κB p65含量比較，差異無統計學意義（P > 0.05）。CTPV組及NF-κB p65抑制組的NF-κB p65含量高于對照組，且NF-κB p65抑制組的NF-κB p65含量低于CTPV組，差異均有統計學意義（均P < 0.05）。經Spearman相關性分析，NF-κB p65與VEGF、TNF-α及ET-1表達均呈正相關（r = 0.620、0.637、0.630，均P < 0.05）。 結論 VEGF、TNF-α、ET-1及NF-κB p65均參與CTPV的發生及發展，且NF-κB p65對VEGF、TNF-α、ET-1具有調控作用，NF-κB p65與VEGF、TNF-α、ET-1表達呈正相關。

[關鍵詞] 核因子-κB；肝門靜脈海綿樣變性；大鼠門靜脈；血管內皮生長因子；腫瘤壞死因子-α；內皮素

[中圖分類號] R-332 [文獻標識碼] A [文章編號] 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.