Carnosic acid inhibits reactive oxygen species-dependent neutrophil extracellular trap formation and ameliorates acute respiratory distress syndrome

中性粒细胞胞外陷阱 急性呼吸窘迫综合征 活性氧 超氧化物 化学 氧化应激 弹性蛋白酶 炎症 超氧化物歧化酶 中性粒细胞弹性蛋白酶 药理学 生物化学 免疫学 生物 医学 内科学
作者
Yung‐Fong Tsai,Shun‐Chin Yang,Yun-Hsuan Hsu,Chun‐Yu Chen,Po‐Jen Chen,Yu-Ting Syu,Ching‐Hsiung Lin,Tsong‐Long Hwang
出处
期刊:Life Sciences [Elsevier BV]
卷期号:321: 121334-121334 被引量:11
标识
DOI:10.1016/j.lfs.2022.121334
摘要

Infiltration of activated neutrophils into the lungs is a hallmark of acute respiratory distress syndrome (ARDS). Neutrophilic inflammation, particularly neutrophil extracellular traps (NETs), is proposed as a useful target for treating ARDS. Carnosic acid (CA) is a food additive; however, its anti-neutrophilic activity in the treatment of ARDS has not been well established. The hypothesis of present study is to confirm that CA alleviates ARDS by suppressing neutrophilic inflammation and oxidative damage.Generation of superoxide anions and reactive oxygen species (ROS), induction of elastase degranulation, and formation of NETs by human neutrophils were assayed using spectrophotometry, flow cytometry, and immunofluorescent microscopy. Immunoblotting was performed to determine the cellular mechanisms involved. Cell-free radical systems were used to test antioxidant activities. The therapeutic effect of CA was evaluated in a lipopolysaccharide (LPS)-induced ARDS mouse model.CA greatly reduced superoxide anion production, ROS production, elastase release, cluster of differentiation 11b expression, and cell adhesion in activated human neutrophils. Mechanistic studies have demonstrated that CA suppresses phosphorylation of extracellular regulated kinase and c-Jun N-terminal kinase in activated neutrophils. CA effectively scavenges reactive oxygen and nitrogen species, but not superoxide anions. This is consistent with the finding that CA is effective against ROS-dependent NET formation. CA treatment significantly improved pulmonary neutrophil infiltration, oxidative damage, NET formation, and alveolar damage in LPS-induced mice.Our data suggested the potential application of CA for neutrophil-associated ARDS therapy.
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