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Salvianolic acid B inhibits myofibroblast transdifferentiation in experimental pulmonary fibrosis via the up-regulation of Nrf2
Liu M(刘苗); Xu, Hanying; Zhang, Ling; Zhang, Cai; Yang, Liancheng; Ma, Enlong; Liu LQ(刘连庆); Li YC(李艳春)
Department机器人学研究室
Source PublicationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN0006-291X
2018
Volume495Issue:1Pages:325-331
Indexed BySCI
WOS IDWOS:000423897600051
Contribution Rank1
Funding OrganizationState Key Laboratory of Robotics, Shenyang Institute of Automation, China Academy of Sciences ; National Natural Science Foundation of China ; Excellent Scholar Projects from the Educational Department of Liaoning Province ; Natural Science Foundation of Liaoning Province ; SPU Excellent Scholar Fund
KeywordPulmonary Fibrosis Mrc-5 Salvianolic Acid b Oxidative Stress Nrf2
AbstractSalvianolic acid B (SalB) is one of the most bioactive components extracted from Salvia miltiorrhiza, and its antioxidant capacity corresponds with its protective effects against cell injury from oxidative stress. The aim of the present study was to evaluate the effect of SalB on experimental pulmonary fibrosis and its ability to ameliorate the oxidative/antioxidative imbalance during fibrosis pathogenesis. The anti fibrotic activity of SalB was first confirmed in Transforming growth factor beta 1(TGF-beta 1)-stimulated MRC-5 cells. The protection of SalB against oxidative stress during fibrogenesis in vitro was verified by detecting ROS production, the levels of glutathione (GSH) and malondialdehyde (MDA). The Western blot and PCR results indicated that SalB could up-regulate nuclear factor erythroid-derived 2-like 2 (Nrf2) at both the protein and mRNA levels and induce Nrf2 nuclear translocation in vitro, which may be the mechanism underlying the anti-fibrotic capacity of SalB. Furthermore, the anti-fibrotic and antioxidant capacities of SalB in vivo were confirmed in rats with BLM-induced pulmonary fibrosis. The immunohistochemistry results showed that Nrf2 was absent in fibroblastic foci (FF) areas, while the SalB treatment could increase the expression of Nrf2 in lung tissues, especially in FF areas. (C) 2017 Elsevier Inc. All rights reserved.
Language英语
WOS SubjectBiochemistry & Molecular Biology ; Biophysics
WOS KeywordOXIDATIVE STRESS
WOS Research AreaBiochemistry & Molecular Biology ; Biophysics
Funding ProjectState Key Laboratory of Robotics, Shenyang Institute of Automation, China Academy of Sciences ; National Natural Science Foundation of China[81470135] ; Excellent Scholar Projects from the Educational Department of Liaoning Province[LJQ2013108] ; Natural Science Foundation of Liaoning Province[2015020722] ; SPU Excellent Scholar Fund
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Document Type期刊论文
Identifierhttp://ir.sia.cn/handle/173321/21530
Collection机器人学研究室
Corresponding AuthorLiu M(刘苗); Li YC(李艳春)
Affiliation1.Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016, China
2.Research Institute of Petrochemical Technology, Liaoning Petrochemical Vocational and Technology College, Jinzhou 121001, China
3.State Key Laboratory of Robotics, Shenyang Institute of Automation, China Academy of Sciences, Shenyang 110016, China
Recommended Citation
GB/T 7714
Liu M,Xu, Hanying,Zhang, Ling,et al. Salvianolic acid B inhibits myofibroblast transdifferentiation in experimental pulmonary fibrosis via the up-regulation of Nrf2[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2018,495(1):325-331.
APA Liu M.,Xu, Hanying.,Zhang, Ling.,Zhang, Cai.,Yang, Liancheng.,...&Li YC.(2018).Salvianolic acid B inhibits myofibroblast transdifferentiation in experimental pulmonary fibrosis via the up-regulation of Nrf2.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,495(1),325-331.
MLA Liu M,et al."Salvianolic acid B inhibits myofibroblast transdifferentiation in experimental pulmonary fibrosis via the up-regulation of Nrf2".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 495.1(2018):325-331.
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