Activation of AMPK attenuates LPS-induced acute lung injury by upregulation of PGC1α and SOD1

Evidence suggests that an imbalance between oxidation and antioxidation is involved in the pathogenesis of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Activation of AMP-activated protein kinase (AMPK) has been shown to inhibit the occurrence of ALI/ARDS. However, it is unknown...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2016-09, Vol.12 (3), p.1551-1555
Main Authors: Wang, Guizuo, Song, Yang, Feng, Wei, Liu, Lu, Zhu, Yanting, Xie, Xinming, Pan, Yilin, Ke, Rui, Li, Shaojun, Li, Fangwei, Yang, Lan, Li, Manxiang
Format: Article
Language:English
Subjects:
acute lung injury
Acute respiratory distress syndrome
AMP-activated protein kinase
Antioxidants
Care and treatment
Development and progression
Enzymes
Gene expression
Genetic aspects
Health aspects
Kinases
Lipid peroxidation
Lipids
Lungs
Neutrophils
Oxidation
Oxidative stress
Pathogenesis
peroxisome proliferator-activated receptor γ coactivator 1α
Properties
Protein kinases
Proteins
Rodents
superoxide dismutase 1
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Summary:Evidence suggests that an imbalance between oxidation and antioxidation is involved in the pathogenesis of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Activation of AMP-activated protein kinase (AMPK) has been shown to inhibit the occurrence of ALI/ARDS. However, it is unknown whether activation of AMPK benefits ALI/ARDS by restoration of the oxidant and antioxidant balance, and which mechanisms are responsible for this process. The present study aimed to address these issues. Lipopolysaccharide (LPS) induced pronounced pathological changes of ALI in mice; these were accompanied by elevated production of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) compared with control mice. Prior treatment of mice with the AMPK agonist metformin significantly suppressed the LPS-induced development of ALI, reduced the elevation of MDA and increased the activity of SOD. Further analysis indicated that activation of AMPK also stimulated the protein expression of peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) and superoxide dismutase 1 (SOD1). This study suggests that activation of AMPK by metformin inhibits oxidative stress by upregulation of PGC1α and SOD1, thereby suppressing the development of ALI/ARDS, and has potential value in the clinical treatment of such conditions.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2016.3465