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目的研究一氧化碳释放分子(CORM)对黏附分子的调节作用,检测一氧化碳(CO)是否能调节炎性介质刺激下血管细胞黏附分子(VCAM)的表达。方法体外培养人脐静脉内皮细胞(HUVEC),分为HUVEC组、HUVEC-TNF-α组(培养液中加入50 ng/mL的TNF-α)、HUVEC-TNF-α-CORM-3组(培养液中加入TNF-α的同时加入1 mmoL CORM-3)。采用流式细胞仪检测细胞VCAM-1的表达;采用电泳迁移率改变分析其对核因子NF-κB活化的影响。将siRNA转染至HUVEC中,采用Western blotting法检测血红素氧合酶(HO-1)的表达,表达成功后,再以TNF-α刺激不加入或加入CORM-3细胞,检测细胞VCAM-1的表达。结果 CORM-3能够抑制由TNF-α刺激后VCAM-1的表达,而释放尽CO的CORM-3则失去了对黏附分子的调控能力;CORM-3能够诱导HO-1的表达,但CORM-3对VCAM-1表达的抑制作用并非由HO-1所介导;CORM-3能够抑制TNF-α诱导的NF-κB通路的激活(P<0.05)。结论降低黏附分子的表达,是抑制炎性反应进程的重要手段。CO对炎性介质刺激下HUVEC细胞VCAM-1表达的调控作用可能是通过其对NF-κB系统的抑制作用实现的。
Objective To investigate the regulatory effect of carbon monoxide releasing molecule (CORM) on adhesion molecules and to determine whether carbon monoxide (CO) regulates the expression of vascular cell adhesion molecule (VCAM) stimulated by inflammatory mediators. Methods Human umbilical vein endothelial cells (HUVECs) were cultured in vitro. The cells were divided into HUVEC group, HUVEC-TNF-α group (50 ng / mL TNF-α and HUVEC-TNF-α-CORM-3 group Add 1 mmoL CORM-3 to the fluid while adding TNF-α). The expression of VCAM-1 was detected by flow cytometry. The effect of NF-κB activation on electrophoretic mobility shift assay was analyzed. The siRNA was transfected into HUVECs and the expression of heme oxygenase (HO-1) was detected by Western blotting. After the expression was successful, CORM-3 cells were not treated with TNF-α or added with VCAM-1 expression. Results CORM-3 could inhibit the expression of VCAM-1 stimulated by TNF-α, whereas CORM-3 with the release of CO lost its ability to regulate adhesion molecules. CORM-3 induced the expression of HO- 3 on the expression of VCAM-1 was not mediated by HO-1. CORM-3 could inhibit the activation of NF-κB induced by TNF-α (P <0.05). Conclusions Decreasing the expression of adhesion molecules is an important way to suppress the progress of inflammatory reaction. The regulation of CO on the expression of VCAM-1 in HUVECs stimulated by inflammatory mediators may be through the inhibition of NF-κB system.