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目的:观察基质金属蛋白酶9(MMP-9)在哮喘大鼠血中性粒细胞(PMN)中的表达及地塞米松对其的影响,探讨血PMN中MMP-9和基质金属蛋白酶抑制剂-1(TIMP-1)的相关性。方法:采用哮喘大鼠模型,随机分成哮喘组、正常对照组、地塞米松治疗组,对血PMN进行分离纯化,免疫细胞化学法检测MMP-9的表达水平,ELISA法检测血清TIMP-1的蛋白浓度。结果:哮喘组(0.196±0.011,OD值)和地塞米松治疗组(0.135±0.008,OD值)中MMP-9的表达水平均显著高于正常对照组(0.100±0.010,OD值)(P<0.01),地塞米松治疗组MMP-9的表达水平显著低于哮喘组(P<0.01)。哮喘组[(34.96±4.54)ng/mL]血清TIMP-1的表达水平分别显著高于正常对照组[(26.14±3.43)ng/mL]和地塞米松治疗组[(29.89±3.43)ng/mL](均P<0.01),地塞米松治疗组TIMP-1的表达水平显著高于正常对照组(P<0.05)。MMP-9与TIMP-1的表达水平呈显著正相关(n=29,r=0.741,P<0.01)。结论:PMN能合成MMP-9,且哮喘时其合成水平增加。PMN可能部分通过MMP-9起作用来参与哮喘的炎症过程,其合成功能可以被地塞米松所抑制。MMP-9及其抑制物TIMP-1共同参与哮喘的发病机制。
Objective: To investigate the expression of matrix metalloproteinase-9 (MMP-9) in asthmatic rat neutrophils (PMN) and the effect of dexamethasone on the expression of MMP-9 and matrix metalloproteinase inhibitor- 1 (TIMP-1). Methods: The asthmatic rat model was randomly divided into asthma group, normal control group and dexamethasone treatment group, the PMN was isolated and purified, the expression of MMP-9 was detected by immunocytochemistry, the expression of TIMP-1 Protein concentration. Results: The expression of MMP-9 in asthma group (0.196 ± 0.011, OD value) and dexamethasone treatment group (0.135 ± 0.008, OD value) were significantly higher than those in the normal control group (0.100 ± 0.010, OD) <0.01). The expression of MMP-9 in dexamethasone group was significantly lower than that in asthma group (P <0.01). The expression of TIMP-1 in asthmatic group [(34.96 ± 4.54) ng / mL] was significantly higher than that in normal control group [(26.14 ± 3.43) ng / mL] and [29.89 ± 3.43 ng / mL] (all P <0.01). The expression of TIMP-1 in dexamethasone group was significantly higher than that in normal control group (P <0.05). There was a significant positive correlation between the expression of MMP-9 and TIMP-1 (n = 29, r = 0.741, P <0.01). Conclusion: PMN can synthesize MMP-9, and the level of synthesis of asthma increased. PMN may participate in the inflammatory process of asthma partly through the action of MMP-9, and its synthesis function can be inhibited by dexamethasone. MMP-9 and its inhibitor TIMP-1 are involved in the pathogenesis of asthma.