Sodium salicylate modulates inflammatory responses through AMP‐activated protein kinase activation in LPS‐stimulated THP‐1 cells

Bao, Weiwei; Luo, Yaru; Wang, Dan; Li, Jian; Xian, Wu; Mei, Wei

doi:10.1002/jcb.26249

Cited by 19 publications

(15 citation statements)

References 46 publications

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“…To further investigate the mechanisms of nuciferine on anti-inflammatory effect, the degradation of IκB-α protein levels were determined with exposure to the nuciferine in the LPS-treated RAW 264.7 cells ( Figure 5 , original results see Figure S2 ). When stimulated only with LPS, the cytosolic IκB-α protein was markedly degraded, consistent with the THP-1 treatment results [ 17 ]. However, nuciferine treatment attenuated the pro-inflammatory effect of the LPS.…”

Section: Resultssupporting

confidence: 83%

Nuciferine Inhibits Proinflammatory Cytokines via the PPARs in LPS-Induced RAW264.7 Cells

et al. 2018

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Inflammation is important and has been found to be an underlying cause in many acute and chronic human diseases. Nuciferine, a natural alkaloid containing an aromatic ring, is found in the nelumbo nucifera leaves. It has been shown to have potential anti-inflammatory activities, but the molecular mechanism has remained unclear. In this study, we found that nuciferine (10 μM) significantly inhibited the lipopolysaccharide (LPS)-induced inflammatory cytokine IL-6 and TNF-α production in RAW 264.7 cells. In addition, the luciferase reporter assay results of different subtypes of the peroxisome proliferator-activated receptor (PPAR) showed that nuciferine dose-dependently activated all the PPAR activities. Specific inhibitors of PPARα and PPARγ significantly abolished the production of inflammatory cytokines as well as IκBα degradation. However, PPARδ inhibitor did not show this effect. Our results suggested a potential molecular mechanism of the anti-inflammatory effects of nuciferine in LPS-induced inflammation, at least in part, by activating PPARα and PPARγ in RAW 264.7 cells.

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Section: Resultssupporting

confidence: 83%

Nuciferine Inhibits Proinflammatory Cytokines via the PPARs in LPS-Induced RAW264.7 Cells

et al. 2018

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“…How does this relationship affect inflammation? Our data showed that AMPK activation not only played an anti-inflammatory role in LPS-induced inflammation ( Figure S1A), as we previously mentioned (15), but also reduced STAT3 phosphorylation ( Figure S1B), similar to other reports (24,25). In addition, we confirmed the pro-inflammatory impact of STAT3 in LPS-stressed macrophages using genetic and pharmacological approaches ( Figure S2).…”

Section: Resultssupporting

confidence: 91%

“…Although previous studies have revealed that STAT3 phosphorylation increases in LPS-stimulated macrophages (24,25), and AMPK regulates STAT3 deactivation [11,16], the exact role of STAT3 in the AMPK-STAT3 regulatory pathway is ambiguous in endotoxin-mediated inflammation. In this study, we assessed the following issues: (1) the timedependent alterations in STAT3 and AMPK activities during LPS-mediated inflammation; (2) the significance of STAT3 in the anti-inflammatory effect of AMPK; (3).…”

Section: Introductionmentioning

confidence: 98%

Nrf2-SHP Cascade-Mediated STAT3 Inactivation Contributes to AMPK-Driven Protection Against Endotoxic Inflammation

et al. 2020

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Signal transducer and activator of transcription 3 (STAT3) is implicated in inflammation processing, but the mechanism of its regulation mostly remains limited to Janus kinase (JAK)-mediated phosphorylation. Although AMP-activated protein kinase (AMPK)-mediated STAT3 inactivation has got documented, the molecular signaling cascade connecting STAT3 inactivation and the anti-inflammatory role of AMPK is far from established. In the present study, we addressed the interplay between AMPK and STAT3, and revealed the important role of STAT3 inactivation in the anti-inflammatory function of AMPK in lipopolysaccharide-stressed macrophages and mice. Firstly, we found that pharmacological inhibition of STAT3 can improve the anti-inflammatory effect of AMPK in wild-type mice, and the expression of STAT3 in macrophage of mice is a prerequisite for the anti-inflammatory effect of AMPK. As to the molecular signaling cascade linking AMPK to STAT3, we disclosed that AMPK suppressed STAT3 not only by attenuating JAK signaling but also by activating nuclear factor erythroid-2-related factor-2 (Nrf2), a redox-regulating transcription factor, which consequently increased the expression of small heterodimer protein (SHP), thus repressing the transcriptional activity of STAT3. In summary, this study provided a unique set of evidence showing the relationship between AMPK and STAT3 signaling and explored a new mechanism of AMPK-driven STAT3 inactivation that involves Nrf2-SHP signaling cascade. These findings expand our understanding of the interplay between pro-and anti-inflammatory signaling pathways and are beneficial for the therapeutic development of sepsis treatments.

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“…Monocyte markers associated with a decreased risk of SIV mac251 acquisition included genes implicated in IL-1β production and regulation ( ANXA2 , EIF4A and IL1RL2 ) and in the suppression of proinflammatory cytokines ( TLR10 and TBK1 ) 22,23 . Gene network inference revealed the importance of hypoxia-inducible factor 1-α (HIF1-α) as a key transcriptional regulator of these protective genes 13,14 (Fig.…”

Section: Resultsmentioning

confidence: 99%

HIV vaccine candidate activation of hypoxia and the inflammasome in CD14+ monocytes is associated with a decreased risk of SIVmac251 acquisition

Vaccari

Fourati

Gordon

et al. 2018

Nat Med

108

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Qualitative differences in the innate and adaptive responses elicited by different HIV vaccine candidates have not been thoroughly investigated. We tested the ability of the Aventis Pasteur live recombinant canarypox vector (ALVAC)–SIV, DNA–SIV and Ad26–SIV vaccine prime modalities together with two ALVAC–SIV + gp120 protein boosts to reduce the risk of SIVmac251 acquisition in rhesus macaques. We found that the DNA and ALVAC prime regimens were effective, but the Ad26 prime was not. The activation of hypoxia and the inflammasome in CD14+CD16− monocytes, gut-homing CCR5-negative CD4+ T helper 2 (TH2) cells and antibodies to variable region 2 correlated with a decreased risk of SIVmac251 acquisition. By contrast, signal transducer and activator of transcription 3 activation in CD16+ monocytes was associated with an increased risk of virus acquisition. The Ad26 prime regimen induced the accumulation of CX3CR1+CD163+ macrophages in lymph nodes and of long-lasting CD4+ TH17 cells in the gut and lungs. Our data indicate that the selective engagement of monocyte subsets following a vaccine prime influences long-term immunity, uncovering an unexpected association of CD14+ innate monocytes with a reduced risk of SIVmac251 acquisition.

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Sodium salicylate modulates inflammatory responses through AMP‐activated protein kinase activation in LPS‐stimulated THP‐1 cells

Cited by 19 publications

References 46 publications

Nuciferine Inhibits Proinflammatory Cytokines via the PPARs in LPS-Induced RAW264.7 Cells

Nuciferine Inhibits Proinflammatory Cytokines via the PPARs in LPS-Induced RAW264.7 Cells

Nrf2-SHP Cascade-Mediated STAT3 Inactivation Contributes to AMPK-Driven Protection Against Endotoxic Inflammation

HIV vaccine candidate activation of hypoxia and the inflammasome in CD14+ monocytes is associated with a decreased risk of SIVmac251 acquisition

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