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目的探讨孟鲁司特通过影响SIL-2R和TNF-α的表达从而引发哮喘患者体内巨噬细胞和T细胞的抗炎症反应的机制。为临床选择用药提供指导。方法对48例轻中度稳定期哮喘患者进行8周孟鲁司特治疗试验,同时选取48列正常成人作为对照。试验前后均测定其1秒量(FEV1)值。同时测定血清中SIL-2R、TNF-α及嗜酸粒细胞阳离子蛋白水平。结果药物治疗后,嗜酸粒细胞阳离子蛋白量明显降低(32.1±11.8VS20.2±11.2,P<0.01),FEV1显著升高(78.9±10.9VS103±13.7,P<0.05)。蛋白水平和检测显示:患者治疗前SIL-2R表达量均显著高于治疗后(1034.77±175.18,773±230.19,P<0.05)及对照组(571.11±123.12;P<0.01)TNF-α表达水平治疗前亦显著高于治疗后与对照组(8.60±1.79,5.89±2.16,5.10±1.07;P<0.05)。Spearman相关分析法分析后显示孟鲁司特疗效与SIL-2RuL及TNF-αTE4有相关性。结论我们的研究显示,孟鲁司特通过降低SIL-2R与TNF-α的表达水平从而引发抗炎症反应。同时,SIL-2R与TNF-α的表达水平亦与孟鲁司特临床疗效密切相关,可作为选择此类药物的参考标志物。
Objective To explore the mechanism of montelukast anti-inflammatory response of macrophages and T cells in asthmatic patients by affecting the expression of SIL-2R and TNF-α. Provide guidance for the clinical choice of medication. Methods 48 patients with mild to moderate stable asthma were treated with montelukast for 8 weeks and 48 normal adults were selected as controls. The one-second amount (FEV1) value was measured before and after the test. Simultaneous determination of serum SIL-2R, TNF-α and eosinophil cationic protein levels. Results After drug treatment, the amount of eosinophil cationic protein was significantly decreased (32.1 ± 11.8 VS20.2 ± 11.2, P <0.01) and FEV1 was significantly increased (78.9 ± 10.9 VS 103 ± 13.7, P <0.05). The levels of SIL-2R in patients before treatment were significantly higher than those in the control group (1034.77 ± 175.18, 773 ± 230.19, P <0.05) and control group (571.11 ± 123.12, P <0.01) Before treatment was also significantly higher than the control group (8.60 ± 1.79,5.89 ± 2.16,5.10 ± 1.07; P <0.05). Spearman correlation analysis showed that the efficacy of montelukast was related to SIL-2RuL and TNF-αTE4. Conclusions Our study shows that montelukast induces an anti-inflammatory response by decreasing the expression level of SIL-2R and TNF-α. Meanwhile, the expression level of SIL-2R and TNF-α is also closely related to the clinical efficacy of montelukast, and can be used as a reference marker for the selection of such drugs.