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Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
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Cx43 Inhibition Attenuates Sepsis-Induced Intestinal Injury via Downregulating ROS Transfer and the Activation of the

Zhaowei Zou1, Bin Liu2, Lisi Zeng3

  • 1Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Mediators of Inflammation
|April 6, 2019
PubMed

Insights

Connexin43 (Cx43) inhibition protects against sepsis-induced intestinal injury by blocking reactive oxygen species (ROS) transfer and the JNK1/Sirt1/FoxO3a pathway. This offers a potential therapeutic strategy for sepsis.

Area of Science:

  • Cell Biology
  • Physiology
  • Pathology

Background:

  • Intestinal injury is central to sepsis pathophysiology.
  • Connexin43 (Cx43) is implicated in sepsis-induced gut damage.

Purpose of the Study:

  • To investigate the role of Cx43 in sepsis-induced intestinal injury.
  • To explore Cx43's potential as a therapeutic target.

Main Methods:

  • Rat cecal ligation and puncture (CLP) model in vivo.
  • LPS-treated IEC-6 cell model in vitro.
  • Cx43 inhibitors, siRNA, ROS scavenger (NAC), JNK1 inhibitor (sp600125), Sirt1 inhibitor (nicotinamide).
  • Luciferase assays and ChIP for gene regulation analysis.

Main Results:

  • Cx43 inhibition attenuated sepsis-induced intestinal injury.
  • Cx43 channels mediate reactive oxygen species (ROS) transfer.
  • Cx43 inhibition affected the JNK1/Sirt1/FoxO3a signaling pathway.
  • FoxO3a directly regulates proapoptotic genes Bim and Puma.

Conclusions:

  • Cx43 inhibition protects against sepsis-induced intestinal injury.
  • Cx43 blockade suppresses ROS transfer and inactivates the JNK1/Sirt1/FoxO3a pathway.

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