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DEXMEDETOMIDINE PREVENTS PDIA3 DECREASE BY ACTIVATING α2-ADRENERGIC RECEPTOR TO ALLEVIATE INTESTINAL I/R IN MICE.

Yaqing Zhan1, Zhaorong Chen, Yuxin Qiu

  • 1Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Shock (Augusta, Ga.)
|November 14, 2022
PubMed
Summary
This summary is machine-generated.

Dexmedetomidine (DEX) protects against intestinal ischemia-reperfusion (I/R) injury by maintaining protein disulfide isomerase A3 (PDIA3) levels via alpha2-adrenergic receptor (α2-AR) activation, reducing inflammation and apoptosis.

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Area of Science:

  • Pharmacology
  • Gastroenterology
  • Cell Biology

Background:

  • Dexmedetomidine (DEX) is known to mitigate intestinal ischemia-reperfusion (I/R) injury.
  • The precise mechanisms underlying DEX's protective effects, particularly its interaction with Protein disulfide isomerase A3 (PDIA3), require further investigation.
  • PDIA3 has emerged as a potential therapeutic target for intestinal I/R injury.

Purpose of the Study:

  • To determine if PDIA3 is involved in the protective effects of DEX against intestinal I/R injury.
  • To elucidate the underlying molecular mechanisms by which DEX confers intestinal protection.
  • To investigate the role of the alpha2-adrenergic receptor (α2-AR) in DEX-mediated intestinal protection.

Main Methods:

  • Utilized PDIA3 Flox/Flox and PDIA3 conditional knockout (cKO) mice to assess PDIA3's role in DEX's protective effects.
  • Induced intestinal I/R injury through superior mesenteric artery occlusion and reperfusion in mouse models.
  • Administered yohimbine, an α2-AR antagonist, to wild-type mice undergoing intestinal I/R to evaluate the involvement of α2-AR.

Main Results:

  • DEX administration significantly attenuated intestinal I/R-induced inflammation, endoplasmic reticulum (ER) stress-dependent apoptosis, and oxidative stress.
  • Deletion of PDIA3 in the intestinal epithelium (cKO) abrogated the protective effects of DEX.
  • Yohimbine treatment reversed DEX's protective effects and reduced PDIA3 expression, indicating α2-AR mediation.

Conclusions:

  • Dexmedetomidine (DEX) exerts protective effects against intestinal I/R injury by preventing the decrease of Protein disulfide isomerase A3 (PDIA3).
  • This protection is mediated through the activation of alpha2-adrenergic receptors (α2-AR).
  • DEX inhibits inflammation, ER stress-induced apoptosis, and oxidative stress in the context of intestinal I/R injury via PDIA3 and α2-AR pathways.