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

doi:https://doi.org/10.1016/J.TAAP.2016.08.004

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

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Abstract

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 dinucleotide phosphate) oxidase-4]. SalB also inhibited the increasing expression of transforming growth factor (TGF)-β1 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-β1/Smad3 signaling. - Highlights: • Salvianolic acid B (SalB) reduced Paraquat-induced mortality and pulmonary injury in mice. • SalB has anti-oxidation,more »« less

Authors:

Liu, Bin ^[1]; Cao, Bo ^[2]; Zhang, Di ^[3]; Xiao, Na ^[1]; Chen, Hong ^[2]; Li, Guo-qiang; Peng, Shou-chun ^[1]; Wei, Lu-qing ^[1]

Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Logistic University of Chinese People's Armed Police Force, Tianjin 300162 (China)
Logistics University of Chinese People's Armed Police Force, Tianjin 300162 (China)
Department of Otorhinolaryngology Head and Neck Surgery, Institute of Otorhinolaryngology, Tianjin First Center Hospital, Tianjin 300192 (China)

Publication Date:: 2016-10-15

OSTI Identifier:: 22690818

Resource Type:: Journal Article

Journal Name:: Toxicology and Applied Pharmacology

Additional Journal Information:: Journal Volume: 309; Other Information: Copyright (c) 2016 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; ADENINES; ASCORBIC ACID; COLLAGEN; DEXAMETHASONE; FIBROSIS; INFLAMMATION; INJURIES; LUNGS; LYMPHOKINES; MICE; MORTALITY; NADP; NICOTINAMIDE; OXIDASES; OXIDATION; PHOSPHORYLATION

Citation Formats


                    Liu, Bin, Cao, Bo, Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Tianjin, 300162, Zhang, Di, Xiao, Na, Chen, Hong, Li, Guo-qiang, Peng, Shou-chun, and Wei, Lu-qing. Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling.  United States: N. p., 2016. 
        Web.  doi:10.1016/J.TAAP.2016.08.004.

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                    Liu, Bin, Cao, Bo, Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Tianjin, 300162, Zhang, Di, Xiao, Na, Chen, Hong, Li, Guo-qiang, Peng, Shou-chun, & Wei, Lu-qing. Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling.  United States.  https://doi.org/10.1016/J.TAAP.2016.08.004

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                    Liu, Bin, Cao, Bo, Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Tianjin, 300162, Zhang, Di, Xiao, Na, Chen, Hong, Li, Guo-qiang, Peng, Shou-chun, and Wei, Lu-qing. Sat .  
        "Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling".  United States.  https://doi.org/10.1016/J.TAAP.2016.08.004.

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@article{osti_22690818,

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

  author       = {Liu, Bin and Cao, Bo and Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Tianjin, 300162 and Zhang, Di and Xiao, Na and Chen, Hong and Li, Guo-qiang and Peng, Shou-chun and Wei, Lu-qing},

  abstractNote = {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 dinucleotide phosphate) oxidase-4]. SalB also inhibited the increasing expression of transforming growth factor (TGF)-β1 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-β1/Smad3 signaling. - Highlights: • Salvianolic acid B (SalB) reduced Paraquat-induced mortality and pulmonary injury in mice. • SalB has anti-oxidation, anti-inflammatory and anti-fibrogenic effects simultaneously. • Its mechanisms were targeting Nrf2-Nox4 redox balance and TGF-β1/Smad3 signaling.},

  doi          = {10.1016/J.TAAP.2016.08.004},

  url          = {https://www.osti.gov/biblio/22690818},
  journal      = {Toxicology and Applied Pharmacology},

  issn         = {0041-008X},

  number       = ,

  volume       = 309,

  place        = {United States},

  year         = {2016},

  month        = {10}

}

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