沙美特罗替卡松对哮喘患者核因子-κB调控单核细胞化学蛋白-1表达的影响

Study of nuclear factor-κB regulating the expression of monocyte chemoactracttive peptide-1 in asthma

目的探讨核因子-κB（NF-κB）及单核细胞化学趋化蛋白-1（MCP-1）在支气管哮喘患者外周血中的表达，并观察用沙美特罗替卡松、布地奈德加沙丁胺醇治疗对其的影响。方法81例哮喘患者随机分为沙美特罗替卡松组（41例）和布地奈德加沙丁胺醇组（40例），另以健康人45例为对照组；用ELISA法测定各组外周血单个核细胞（PBMC）中NF-κB活性和MCP-1水平。结果①沙美特罗替卡松治疗组PBMC中NF-κB活性[（1．32±0．36）ng／L]及MCP-1水平[（66．89±5．62）ng／L]和布地奈德加沙丁胺醇治疗组PBMC中NF-κB活性[（1．70±0．39）ng／L]及MCP-1水平[（73．35±7．52）ng／L]明显高于正常对照组[（0．89±0．34）ng／L及（58．63±8．24）ng／L，P均〈0．001]；②沙美特罗替卡松治疗组PBMC中NF-κB活性和MCP-1水平明显低于布地奈德加沙丁胺醇治疗组（P均〈0．001）。结论NF-κB基因及其调控蛋白MCP—1参与了哮喘的发病过程，激素和B2受体激动剂联用治疗后可延缓哮喘的发病。

Objective To explore the expression of the nuclear factor -κB （NF-κB） regulating monocyte chemoactracttive peptide -1 （ MCP-1 ） in asthma patients, and investigate the effect of seretide, hudesonide and ventolin. Methods 81 asthma patients were randomly divided into seretide therapy group and budesonide and ventolin therapy group. The NF-κB activation in PBMC and the plasma concentrations of MCP-1 were measured by ELISA. Results （1）The NF-κB activation in PBMC of seretide therapy group （ 1.32 ± 0.36） ng/L and in budesonide and ventolin therapy group （ 1.70 ± 0.39） ng/L of asthma patients were significantly higher than that control group （0.89 ± 0.34） ng/L （P 〈 0.001 ） ; The plasma MCP-1 level in seretide therapy group （ 66.89 ± 5.62） ng/L and in budesonide and ventolin therapy group （73.35 ± 7.52） ng/L of asthma patients were also significantly higher than that in control group （58.63± 8.24）ng/L, （P 〈 0.001 ）. （2）The NF-κB activation in PBMC and the plasma MCP-1 level of seretide therapy group in asthma patients were significantly lower than budesonide and ventolin therapy group （P 〈 0.001 ）. Conclusion NF-κB gene and its regulating protein MCP-1 may be involved in asthma. Glucocotiosteroid and beta2 agonists combination may prolong the process of asthma.