Arbutin attenuates LPS-induced lung injury via Sirt1/ Nrf2/ NF-κBp65 pathway

被引：58

作者：

Ye, Jinyan ^{[1
,2
]}

Guan, Minqiang ^{[3
]}

Lu, Yao ^{[2
]}

Zhang, Dan ^{[2
]}

Li, Chengye ^{[2
]}

Zhou, Caicun ^{[1
,4
]}

机构：

[1] Soochow Univ, Affiliated Hosp 3, Changzhou 213000, Peoples R China

[2] Wenzhou Med Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Wenzhou 325000, Peoples R China

[3] Wenzhou Med Univ, Lab Anim Ctr, Wenzhou 325000, Peoples R China

[4] Tongji Univ, Shanghai Pulm Hosp, Sch Med, Dept Oncol, Shanghai 200433, Peoples R China

来源：

PULMONARY PHARMACOLOGY & THERAPEUTICS | 2019年 / 54卷

关键词：

Arbutin; SIRT1; Lipopolysaccharide; Lung injury; NF-KAPPA-B; INFLAMMATION; INVOLVEMENT; ACTIVATION; EXPRESSION; CROSSTALK; SYSTEM;

D O I：

10.1016/j.pupt.2018.12.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The main goal of this study was to evaluate the effects of arbutin (AR) on lipopolysaccharide (LPS)-induced lung injury. A lung injury rat model was established by intravenous LPS administration. We found that levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) in both serum and lung tissue were significant increased after LPS challenge. In addition, pathological conditions were examined in rat lungs, and it was demonstrated that AR-pretreatment reduced LPS-induced malondialdehyde (MDA) levels and increased LPS-induced superoxide dismutase (SOD) activity. Moreover, the expression of sirtuin1 (SIRT1), nuclear erythroid factor 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1) as well as the phosphorylation of NF-kappa Bp65 and I kappa B alpha were increased with LPS-induced lung injury, and were significantly restored by AR treatment. Together, our results indicated that SIRT1 is a potential therapeutic target in LPS-induced lung injury, and that AR may be a novel therapeutic in patients with acute lung injury.

引用

页码：53 / 59

页数：7

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