Astragalin reduces lipopolysaccharide-induced acute lung injury in rats via induction of heme oxygenase-1
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Online ISSN 1976-3786 Print ISSN 0253-6269
RESEARCH ARTICLE
Astragalin reduces lipopolysaccharide-induced acute lung injury in rats via induction of heme oxygenase-1 Donghua Zheng1 • Dawei Liu2 • Na Liu1 • Yukun Kuang3 • Qiang Tai1
Received: 2 February 2019 / Accepted: 14 June 2019 The Pharmaceutical Society of Korea 2019
Abstract Astragalin, a bioactive component of medicinal plants such as Rosa agrestis, has anti-inflammatory and antioxidant features. Induction of heme oxygenase (HO)-1 is an effective strategy to reduce excessive generated oxidants during the pathogenesis of acute lung injury (ALI). The aim of the present study is to investigate that whether the anti-inflammatory and antioxidant features of astragalin is HO-1 dependent in lipopolysaccharide (LPS)-induced ALI. Sprague–Dawley rats were used in animal study. Intratracheal LPS was performed to induce experimental ALI model. Astragalin was administrated 1 h after LPS challenge. Human lung epithelial cells were used in cell study. Samples from rats were harvested at 24 h post LPS challenge. Astragalin treatment inhibited LPS-induced inflammatory cells infiltration in the lung and pulmonary edema. Astragalin treatment markedly enhanced the activity of HO-1 compared with vehicle-treated group at 24 h post LPS challenge. Levels of lipid hydroperoxide, a marker for oxidative stress, were decreased in astragalintreated animals compared with vehicle-treated group. However, the protective effect of astragalin on LPS-induced ALI was abolished in an inhibitor of HO-1-treated Donghua Zheng and Dawei Liu have contributed equally to this work. & Qiang Tai [email protected] 1
Department of Critical Care Medicine, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Er Road, Guangzhou 510000, GuangDong, China
2
Department of Pathology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, GuangDong, China
3
The Division of Pulmonary and Critical Care Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, GuangDong, China
animals. Moreover, the astragalin-induced the upregulation of HO-1 in human lung epithelial cells was inhibited when nuclear factor erythroid-2-related factor 2 (Nrf2) was silenced by small interfering RNA. Astragalin reduces LPS-induced ALI via activation of Nrf2/HO-1 pathway. Keywords Astragalin Acute lung injury HO-1 Nrf2
Introduction Acute respiratory distress syndrome (ARDS), a severe inflammatory disorder of the lungs, is a common complication of sepsis (Sweeney and McAuley 2016). During the pathogenesis of sepsis, a number of activated neutrophils transmigrate and infiltrate into the lungs to eliminate invading pathogens via releasing oxidants and proteolytic enzymes, such as myeloperoxidase (MPO) and matrix metalloprotease (MMP) (Sweeney and McAuley 2016). However, excessive released oxidants, proinflammatory mediators, and proteolytic enzymes by activated neutrophils may cause lung injury (Sweeney and McAuley 2016). A great effort has been made to reduce ARD
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