Objective To study the association between serum level of high-mobility group box 1(HMGB1) and neonatal respiratory distress syndrome (NRDS). Methods A total of 35 infants with NRDS and 35 normal neonates (control group) were enrolled. Peripheral venous blood samples were collected with 12-24 hours after birth. ELISA was used to measure the serum level of HMGB1. Results The infants with mild and severe NRDS had a significantly higher serum level of HMGB1 than the control group (P < 0.05). The infants with severe NRDS had a significantly higher serum level of HMGB1 than those with mild NRDS (P < 0.05). The infants with NRDS who died had a significantly higher serum level of HMGB1 than those who survived (P < 0.05). The receiver operating characteristic (ROC) curve showed that the optimal cut-off value for serum level of HMGB1 to predict NRDS was 625.3 pg/mL with an area under the ROC curve (AUC) of 0.846 (95%CI:0.755-0.936), and the optimal cut-off value for serum level of HMGB1 to predict the death of infants with NRDS was 772.2 pg/mL with an AUC of 0.916 (95%CI:0.813-1.000). Conclusions Infants with NRDS have a significant increase in the serum level of HMGB1, and the serum level of HMGB1 can well predict the development and prognosis of NRDS.
WANG Wen-Xiu, CHEN Bo, ZHANG Wei, ZHANG Hui-Rong.
Association between high-mobility group box 1 and neonatal respiratory distress syndrome[J]. Chinese Journal of Contemporary Pediatrics. 2017, 19(4): 398-401 https://doi.org/10.7499/j.issn.1008-8830.2017.04.007
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
[1] Speer CP. Neonatal respiratory distress syndrome:an inflammatory disease?[J]. Neonatology, 2011, 99(4):316-319. [2] Bhargava R, Janssen W, Altmann C, et al. Intratracheal IL-6 protects against lung inflammation in direct, but not indirect, causes of acute lung injury in mice[J]. PLoS One, 2013, 8(5):e61405. [3] Zhao H, Zhang J, Yu J. HMGB-1 as a potential target for the treatment of diabetic retinopathy[J]. Med Sci Monit, 2015, 21:3062-3067. [4] Zhou H, Ji X, Wu Y, et al. A dual-role of Gu-4 in suppressing HMGB1 secretion and blocking HMGB1 pro-inflammatory activity during inflammation[J]. PLoS One, 2014, 9(3):e89634. [5] Li Y, Xiang M, Yuan Y, et al. Hemorrhagic shock augments lung endothelial cell activation:role of temporal alterations of TLR4 and TLR2[J]. Am J Physiol Regul Integr Comp Physiol, 2009, 297(6):R1670-R1680. [6] Liu Z, Liu J, Wang J, et al. Role of testis-specific high-mobilitygroup protein in transcriptional regulation of inducible nitric oxide synthase expression in the liver of endotoxic shock mice[J]. FEBS J, 2014, 281(9):2202-2213. [7] Yang Q, Liu X, Yao Z, et al. Penehyclidine hydrochloride inhibits the release of high-mobility group box 1 in lipopolysaccharide-activated RAW264.7 cells and cecal ligation and puncture-induced septic mice[J]. J Surg Res, 2014, 186(1):310-317. [8] Musumeci D, Roviello GN, Montesarchio D. An overview on HMGB1 inhibitors as potential therapeutic agents in HMGB1-related pathologies[J]. Pharmacol Ther, 2014, 141(3):347-357. [9] 孙波. 呼吸系统疾病[M]//邵肖梅, 叶鸿瑁, 丘小汕. 实用新生儿学. 第4版. 北京:人民卫生出版社, 2011:395-398. [10] Qian L, Liu C, Zhuang W, et al. Neonatal respiratory failure:a 12-month clinical epidemiologic study from 2004 to 2005 in China[J]. Pediatrics, 2008, 121(5):e1115-e1124. [11] Britt RD, Jr, Velten M, Tipple TE, et al. Cyclooxygenase-2 in newborn hyperoxic lung injury[J]. Free Radic Biol Medicine, 2013, 61:502-511. [12] Sarafidis K, Drossou-Agakidou V, Kanakoudi-Tsakalidou F, et al. Evidence of early systemic activation and transendothelial migration of neutrophils in neonates with severe respiratory distress syndrome[J]. Pediatr Pulmonol, 2001, 31(3):214-219. [13] Lyra PP, Diniz EM, Abe-Sandes K, et al. Surfactant protein B gene polymorphism in preterm babies with respiratory distress syndrome[J]. Braz J Med Biol Res, 2011, 44(1):66-72. [14] Hamvas A, Heins HB, Guttentag S H, et al. Developmental and Genetic Regulation of Human Surfactant Protein B in vivo[J]. Neonatology, 2008, 95(2):117-124. [15] 曾凌空, 李文斌, 潘睿, 等. 肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的研究[J]. 中国循证儿科杂志, 2011, 6(1):37-41. [16] Ferhani N, Letuve S, Kozhich A, et al. Expression of highmobility group box 1 and of receptor for advanced glycation end products in chronic obstructive pulmonary disease[J]. Am J Respir Crit Care Med, 2010, 181(9):917-927. [17] 王贵佐, 卢家美, 谢新明, 等. 过氧化物酶体增殖物激活受体在肺部疾病中的作用[J]. 中国药理学通报, 2013, 29(1):18-22. [18] Ebina M, Taniguchi H, Miyasho T, et al. Gradual increase of high mobility group protein b1 in the lungs after the onset of acute exacerbation of idiopathic pulmonary fibrosis[J]. Pulm Med, 2011, 2011:916486.