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

Wang, Guizuo; Song, Yang; Feng, Wei; Liu, Lu; Zhu, Yanting; Xie, Xinming; Pan, Yilin; Rui, Ke; Li, Shaojun; Li, Fangwei; Yang, Lan; Li, Manxiang

doi:10.3892/etm.2016.3465

Cited by 48 publications

(37 citation statements)

References 22 publications

(28 reference statements)

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“…Taken together, these data demonstrate a beneficial effect of AMPK activation in younger mice, greater than that in older mice, and suggest that the AICAR's beneficial effects were a result of AMPK activation, rather than off-target effects. This work extends the similar prior findings of the role of AMPK in LPS-induced lung injury (7,8) to hemorrhage-induced lung injury.…”

Section: Impaired Ampk Activity Drives Age-associated Acute Lung Injusupporting

confidence: 88%

Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage

Southern

Scheraga

Olman

2017

Am J Respir Cell Mol Biol

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Section: Impaired Ampk Activity Drives Age-associated Acute Lung Injusupporting

confidence: 88%

Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage

Southern

Scheraga

Olman

2017

Am J Respir Cell Mol Biol

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“…A recent study has reported that the level of PGC‐1α was reduced in a murine model of ALI . In our current study, ALI mouse model was established by injection of LPS to explore the potential roles of PGC1α/HSF1 and its underlying molecular mechanism.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome proliferator‐activated receptor gamma coactivator‐1α/HSF1 axis effectively alleviates lipopolysaccharide‐induced acute lung injury via suppressing oxidative stress and inflammatory response

Dang¹,

Du²,

Hu³

et al. 2018

J of Cellular Biochemistry

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Acute lung injury (ALI) interferes with lung function by causing pulmonary inflammation and oxidative stress. Suppressing intracellular reactive oxygen species (ROS) may block intracellular inflammation. Thus, the purpose of the current study was to investigate the roles of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α)/HSF1 axis in an lipopolysaccharide (LPS)-induced ALI murine model and in RAW264.7 macrophages. In the LPS-administrated mouse model, the addition of PGC1α obviously ameliorated secretion of pro-inflammatory mediators tumor necrosis factor-α and Interleukin 6 as well as MCP-1 expression triggered by LPS stimulation, accompanied with reduced infiltration of inflammatory cells. Meanwhile, introduction of PGC1α strongly diminished the expression of cyclooxygenase-2 and inducible nitric oxide synthase as well as their products PGE2 and NO. In addition, administering PGC1α also dramatically alleviated LPS-triggered oxidative stress, as reflected by a reduction of ROS production, and also reduced malondialdehyde and O content, concomitant with enhancement of superoxide dismutase, catalase, and glutathione peroxidase. Similarly, PGC1α effectively ameliorated LPS-induced inflammation response and oxidative stress, as exemplified by reduced pro-inflammatory cytokines and ROS production in LPS-induced RAW264.7 macrophages. Interestingly, PGC1α modulated the expression of HSF1 and the transcriptional activity of X-linked inhibitor of apoptosis (XIAP)-associated factor 1, whereas silencing of HSF1 abolished these effects. More importantly, deletion of HSF1 impeded the anti-inflammatory and anti-oxidant effects of PGC1α in LPS-induced macrophages. Taken together, PGC1α/HSF1 axis have an anti-oxidant and anti-inflammatory effects, indicating that PGC1α/HSF1 may protect against LPS-induced ALI, and thus may be a promising therapy to treat ALI.

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“…In this study, AL treatment decreased the MDA content. SOD is an important antioxidant that can eliminate the harmful byproducts of cellular metabolisms, such as free radicals . Our results indicated that AL treatment increased SOD levels over those observed in the untreated LPS‐injured group.…”

Section: Discussionmentioning

confidence: 53%

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

Lin

Hou

et al. 2019

J Biochem & Molecular Tox

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We investigated the effects and associated mechanism of alkannin (AL) on lipopolysaccharide (LPS)-induced acute lung injury in a mouse model. Pretreatment with AL in vivo significantly reduced the lung wet/dry weight ratio and inhibited lung myeloperoxidase activity and malondialdehyde content, while increasing superoxide dismutase activity. Hematoxylin and eosin staining demonstrated that AL attenuated lung histopathological changes. In addition, AL-inhibited overproduction of proinflammatory cytokines in bronchoalveolar lavage fluid and lung tissues in LPS-injured mice and LPS-exposed A549 cells. Further analysis showed that AL-inhibited induction of the Rho/ROCK/NF-κB pathway via LPS-induced inflammation in mice and A549 cells. Fasudil, a selective ROCK inhibitor, showed similar effects. Overall, the findings indicate that AL suppresses the expression of messenger RNAs and proteins associated with Rho/ROCK/NF-κB signaling to effectively ameliorate lung injury. K E Y W O R D S alkannin, lipopolysaccharide, lung injury, Rho/ROCK/NF-κB

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

Cited by 48 publications

References 22 publications

Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage

Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage

Peroxisome proliferator‐activated receptor gamma coactivator‐1α/HSF1 axis effectively alleviates lipopolysaccharide‐induced acute lung injury via suppressing oxidative stress and inflammatory response

Alkannin attenuates lipopolysaccharide‐induced lung injury in mice via Rho/ROCK/NF‐κB pathway

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