Luteolin Suppresses Sepsis-Induced Cold-Inducible RNA-Binding Protein Production and Lung Injury in Neonatal Mice

新生儿败血症 腹腔注射 促炎细胞因子 败血症 细胞因子 化学 木犀草素 下调和上调 炎症 医学 药理学 免疫学 男科 内科学 生物化学 类黄酮 抗氧化剂 基因
作者
Yuanyuan Zhang,Jia Zhang,Yifan Ren,Teng Li,Jianbin Bi,Zhaoqing Du,Rongqian Wu
出处
期刊:Shock [Ovid Technologies (Wolters Kluwer)]
卷期号:55 (2): 268-273 被引量:21
标识
DOI:10.1097/shk.0000000000001624
摘要

ABSTRACT Neonatal sepsis is a life-threatening inflammatory condition. Extracellular cold-inducible RNA-binding protein (CIRP), a proinflammatory mediator, plays a critical role in the pathogenesis of sepsis-induced lung injury in neonates. Luteolin, a polyphenolic flavonoid, has potent anti-inflammatory properties. However, the effects of luteolin on CIRP production and neonatal sepsis-induced lung injury remained unknown. We therefore hypothesize that treatment with luteolin suppresses CIRP production and attenuates lung injury in neonatal sepsis. To study this, sepsis was induced in C57BL/6J mouse pups (5–7 days) by intraperitoneal cecal slurry injection (CSI). One hour after CSI, luteolin (10 mg/kg body weight) or vehicle (normal saline) was administered through intraperitoneal injection. CIRP mRNA and protein were determined and lung injury was assessed at 10 h after CSI. Our results showed that administration of luteolin decreased CIRP mRNA and protein, improved lung architecture, reduced lung edema, and apoptosis after CSI. To examine the direct effect of luteolin on CIRP production, peritoneal macrophages were isolated from neonatal mice and stimulated with 100 ng/mL LPS with or without the presence of luteolin. The result indicates that luteolin directly inhibited LPS-induced CIRP production in neonatal macrophages. In addition, luteolin also downregulated hypoxia-inducible factor-1α (HIF-1α) and NOD-like receptor 3 (NLRP3) expression in septic neonates and in LPS-stimulated neonatal macrophages. In conclusion, administration of luteolin suppresses CIRP production and attenuates lung injury in neonatal sepsis. The beneficial effect of luteolin may be related to downregulation of HIF-1α and NLRP3 expression in neonatal macrophages. Luteolin may be developed as an adjunctive therapy for neonatal sepsis.
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