输血相关急性肺损伤SD大鼠血管生成素2和白介素10的变化

目的分析患输血相关急性肺损伤(TRALI)的SD大鼠肺组织中血管生成素2(Ang-2)和白介素10(IL-10)基因相对表达量与血浆、肺组织Ang-2、IL-10浓度变化。方法 SD大鼠20只,随机分为TRALI组(n=10):腹腔注射脂多糖(LPS)(2 mg/kg)2 h后静脉输注人血浆(约1 mL/只);正常对照组(n=5):采用假手术处理;阳性对照组(n=5):静脉输注LPS(5 mg/kg)诱导急性肺损伤。应用实时荧光定量RT-PCR检测大鼠肺组织Ang-2、IL-10基因相对表达量,以管家基因b-actin为对照,2-(△△Ct)法计算目的基因相对表达情况;应用ELISA法检测大鼠血浆、肺组织中Ang-2和IL-10浓度。结果与正常对照组肺组织Ang-2、L-10基因相对表达量相比,TRALI组肺组织Ang-2基因相对表达量下调(0.28±0.06),IL-10基因相对表达量上调(22.40±1.19)。TRALI组血液、肺组织中Ang-2和IL-10浓度分别为(133.83±0.81)、(22.81±0.40)和(106.54±1.92)、(33.35±6.84)(mg/L),较正常对照组上升(P<0.05)。结论 TRALI SD大鼠血浆、肺组织中Ang-2、IL-10浓度明显高于正常对照SD大鼠,随TRA-LI病程发展,IL-10逐渐发挥其拮抗炎症作用,对Ang-2基因表达可能有反馈抑制作用。

Change of angiopoietin-2 and intedeukin-10 on transfusion-related acute lung injury in Sprague Dawley rat

Objective To study the change of gene expression in lung and concentration in plasma and lung of Ang-2 and IL-10 in rats with transfusion-related acute lung injury(TRALI).Methods A total of 20 SD rats were randomly divided into control group(n = 5) with sham operation,positive control group(n = 5) with ALl induced by intravenous infusion of LPS(5 mg / kg),and TRALI group(n = 10) treated by intraperitoneal injection of LPS 2 h before the transfusion of human plasma(about 1 mL).Gene expression in Ang-2 and IL-10 was detected by real-time fluorescent qualification RT-PCR on the control of b-actin(housekeeping gene).The method of 2-(△△Ct) was used to calculate the relative qualification of target genes.Results Compared with gene expression of Ang-2 and IL-10 of normal group,the gene expression of Ang-2 was downregulated(0.28 ± 0.06) and gene expression of IL-10 was upregulated(22.40 ± 1.19) in the lung tissue of TRALI group.The concentration of Ang-2 and IL-10 was higher in TRALI group(133.83 ± 0.81),(22.81 ± 0.40) and(106.54 ± 1.92),(33.35 ± 6.84)(mg / L) than that in the normal group.Conclusion The concentration of Ang-2 in the plasma and lung of rats in TRALI group was significantly higher than that in normal group.In the development course of TRALI,IL10 in plasma may inhibit the gene expression of Ang-2 in lung.