Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling

被引:49
作者
Liu, Bin [1 ]
Cao, Bo [2 ,3 ]
Zhang, Di [4 ]
Xiao, Na [1 ]
Chen, Hong [2 ]
Li, Guo-qiang [1 ]
Peng, Shou-chun [1 ]
Wei, Lu-qing [1 ]
机构
[1] Logist Univ Chinese Peoples Armed Police Force, Affiliated Hosp, Dept Resp & Crit Care Med, Tianjin 300162, Peoples R China
[2] Logist Univ Chinese Peoples Armed Police Force, Tianjin 300162, Peoples R China
[3] Tianjin Key Lab Cardiovasc Remodeling & Target Or, Tianjin 300162, Peoples R China
[4] Tianjin First Ctr Hosp, Inst Otorhinolaryngol, Dept Otorhinolaryngol Head & Neck Surg, Tianjin 300192, Peoples R China
关键词
Paraquat; Salvianolic acid B; Pulmonary fibrosis; Nrf2; NOX4; TGF-beta 1/Smad3 signaling pathway; OXIDATIVE STRESS; GLUTATHIONE REDOX; NADPH OXIDASE; LUNG FIBROSIS; UP-REGULATION; TOXICITY; DYSFUNCTION; MECHANISMS; BLEOMYCIN; DISEASE;
D O I
10.1016/j.taap.2016.08.004
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The present study was aimed at exploring the protective effects of Salvianolic acid B (SalB) against paraquat (PQ) induced lung injury in mice. Lung fibrotic injuries were induced in mice by a single intragastrical administration of 300 mg/kg PQ then the mice were administrated with 200 mg/kg, 400 mg/kg SalB, 100 mg/kg vitamin C (Vit C) and dexamethasone (DXM) for 14 days. PQ-triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release, and oxidative stress damages in lung tissues and mortality of mice were attenuated by SalB in a dose-dependent manner. Furthermore, SalB was noted to enhance the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and reduce expression of the reactive oxygen species-generating enzyme Nox4 [NADPH (reduced form of nicotinamide adenine di nucleotide phosphate) oxidase-4]. SalB also inhibited the increasing expression of transforming growth factor (TGF)-beta 1 and the phosphorylation of its downstream target Smad3 which were enhanced by PQ These results suggest that SalB may exert protective effects against PQ-induced lung injury and pulmonary fibrosis. Its mechanisms involve the mediation of Nrf2/Nox4 redox balance and TGF-beta 1/Smad3 signaling. (C) 2016 Published by Elsevier Inc.
引用
收藏
页码:111 / 120
页数:10
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