脂氧素A4在结核性胸膜纤维化中的表达水平及影响机制初探

目的分析脂氧素A4 (LXA4)在结核性胸膜炎患者胸膜纤维化进程中的表达水平及影响机制。方法收集山东大学附属山东省胸科医院2017年7月至2018年12月收治的61例结核性胸腔积液患者和15例癌性胸腔积液患者的临床资料,按有无胸膜纤维化分为结核纤维化组(27例)、结核无纤维化组(34例)和癌性无纤维化组(15例),检测各组胸腔积液中LXA4的浓度,进行对比分析;并对结核性胸腔积液患者的LXA4及转化生长因子β(TGF-β)进行相关性分析。结果结核无纤维化组LXA4浓度的中位数(四分位数)M(Q1,Q3)]为7.74(4.69,10.55) ng/L,明显低于结核纤维化组12.50(11.60,14.83) ng/L],差异有统计学意义(Z=-3.830,P<0.001)。癌性无纤维化组LXA4浓度为7.88(5.91,15.02) ng/L,与结核无纤维化组7.74(4.69,10.55) ng/L]比较,差异无统计学意义(Z=-0.586,P=0.558)。61例结核性胸腔积液患者LXA4浓度10.23(5.14,13.15) ng/L]与TGF-β浓度46.30 (41.04,60.85) ng/L]呈负相关性(Spearman相关系数检验,rs=-0.519,P<0.001)。结论 LXA4在结核性胸膜炎胸膜纤维化患者中存在高表达,且与TGF-β呈明显负相关性,可能为通过抑制TGF-β而发挥抗胸膜纤维化的作用。

Exploration of the expression level of lipoxin A4 and its influence mechanism in process of tuberculous pleural fibrosis

Objective To analyze the expression level of lipoxin A4 (LXA4) and its influence mechanism in the process of pleural fibrosis in the patients with tuberculous pleurisy. Methods The clinical data of 61 patients with tuberculous pleural effusion and 15 patients with cancerous pleural effusion, who were treated at Shandong Provincial Chest Hospital Affiliated to Shandong University from July 2017 to December 2018, were collected. According to presence or absence of pleural fibrosis, the enrolled patients were divided into three groups: tuberculous pleural fibrosis group (27 cases), tuberculous without pleural fibrosis group (34 cases) and cancerous without pleural fibrosis group (15 cases). The LXA4 concentration in the pleural effusion of the patients in each group was tested and compared; the correlation between LXA4 and TGF-β in the tuberculous pleural effusion was analyzed. Results The median (quartile) of LXA4 concentration was 7.74 (4.69, 10.55) ng/L in the patients of tuberculous without pleural fibrosis group, which was statistically significant lower than that in the patients of tuberculous pleural fibrosis group (12.50 (11.60, 14.83) ng/L; Z=-3.830, P<0.001). The concentration of LXA4 was 7.88 (5.91, 15.02) ng/L in the patients of cancerous without pleural fibrosis group, there was no significant difference compared with the tuberculosis patients without pleural fibrosis (Z=-0.586, P=0.558). The concentrations of LXA4 (10.23 (5.14, 13.15) ng/L) and TGF-β (46.30 (41.04, 60.85) ng/L) were negative correlation in 61 tuberculosis patients with pleural effusion (Spearman correlation coefficient, r_s=-0.519, P<0.001). Conclusion The LXA4 concentration is highly expressed in tuberculous pleurisy patients with pleural fibrosis, and has a significant negative correlation with the concentration of TGF-β. It may play an anti pleural fibrosis role by inhibiting TGF-β.