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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.
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页码:111 / 120
页数:10
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