Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

PeerJ

article

Xue Liu¹  Huaman Liu³  Yi Zhai⁴  Yan Li⁵  Xue Zhu³  Wei Zhang³ 

[1] College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine;Department of Respiration, Shandong Provincial Chest Hospital;Department of Respiration, Affiliated Hospital of Shandong University of Traditional Chinese Medicine;Medical Department, Affiliated Hospital of Shandong University of Traditional Chinese Medicine;Department of Nursing, Zibo Central Hospital

关键词: Laminarin;    Pulmonary oxidative damage;    Pulmonary fibrosis;    Hydrogen peroxide;    NRF2;   

DOI  :  10.7717/peerj.3642

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Oxidative damage is a major cause of lung diseases, including pulmonary fibrosis. Laminarin is a kind of polysaccharide extracted from brown algae and plays vital roles in various biological processes. However, the functions and mechanisms of laminarin in pulmonary oxidative damage are poorly understood. This study aimed at investigating the protective effect of laminarin against pulmonary oxidative damage and underlying mechanisms. Human lung fibroblasts MRC-5 cells were treated with hydrogen peroxide to induce oxidative damage. Laminarin treatment was performed before or after hydrogen peroxide treatment, and then major indexes of oxidative damage, including superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH) and catalase (CAT), were quantified by biochemical assays. The expression of oxidation-related factor, nuclear factor erythroid 2 like 2 (NRF2) was analyzed by qPCR, Western blot and immunofluorescence assay. NRF2 knockdown and overexpression were performed by cell transfection to reveal possible mechanisms. Results showed that laminarin treatment of 0.020 mg/mL for 24 h, especially the pre-treatment, could significantly relieve changes in SOD, MDA, GSH and CAT that were altered by hydrogen peroxide, and promote NRF2 mRNA (P < 0.001). NRF2 protein was also elevated by laminarin, and nuclear translocation was observed. Factors in NRF2 signaling pathways, including KEAP1, NQO1, GCLC and HO1, were all regulated by laminarin. Roles of NRF2 were tested, suggesting that NRF2 regulated the concentration of SOD, MDA, GSH and CAT, suppressed KEAP1, and promoted NQO1, GCLC and HO1. These findings suggested the protective role of laminarin against pulmonary oxidative damage, which might involve the regulation of NRF2 signaling pathways. This study provided information for the clinical application of laminarin to pulmonary diseases like pulmonary fibrosis.

【 授权许可】

CC BY