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
收藏
页码：53 / 59
页数：7
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