salidroside inhibits hmgb1 acetylation and release through upregulation of sirt1 during inflammation

Clicks: 208
ID: 255813
2017
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #90 of 359 articles by views in journal of aoac international

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 359 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
HMGB1, a highly conserved nonhistone DNA-binding protein, plays an important role in inflammatory diseases. Once released to the extracellular space, HMGB1 acts as a proinflammatory cytokine that triggers inflammatory reaction. Our previous study showed that salidroside exerts anti-inflammatory effect via inhibiting the JAK2-STAT3 signalling pathway. However, whether salidroside inhibits the release of HMGB1 is still unclear. In this study, we aim to study the effects of salidroside on HMGB1 release and then investigate the potential molecular mechanisms. In an experimental rat model of sepsis caused by CLP, salidroside administration significantly attenuated lung injury and reduced the serum HMGB1 level. In RAW264.7 cells, we investigated the effects of salidroside on LPS-induced HMGB1 release and then explored the underlying molecular mechanisms. We found that salidroside significantly inhibited LPS-induced HMGB1 release, and the inhibitory effect was correlated with the HMGB1 acetylation levels. Mechanismly, salidroside inhibits HMGB1 acetylation through the AMPK-SirT1 pathway. In addition, SirT1 overexpression attenuated LPS-induced HMGB1 acetylation and nucleocytoplasmic translocation. Furthermore, in SirT1 shRNA plasmid-transfected cells, salidroside treatment enhanced SirT1 expression and reduced LPS-activated HMGB1 acetylation and nucleocytoplasmic translocation. Collectively, these results demonstrated that salidroside might reduce HMGB1 release through the AMPK-SirT1 signalling pathway and suppress HMGB1 acetylation and nucleocytoplasmic translocation.
Reference Key
qi2017oxidativesalidroside Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Zhilin Qi;Yao Zhang;Shimei Qi;Liefeng Ling;Lin Gui;Liang Yan;Jun Lv;Qiang Li
Journal journal of aoac international
Year 2017
DOI
10.1155/2017/9821543
URL
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.