Dexmedetomidine activates the PKA/CREB pathway and inhibits proinflammatory factor expression through β2 adrenergic receptors.

ABSTRACT:

Introduction

Dexmedetomidine (DEX) is primarily utilized for sedation in the context of general anesthesia or intensive care. However, the exact regulatory mechanism by which DEX affects cytokines remains unclear. This study aims to investigate the underlying mechanism by which DEX inhibits proinflammatory factors through activation of the β2 adrenergic receptor (β2 AR).

Methods

The inflammatory cell model of human mononuclear macrophage (THP-1) cells induced by lipopolysaccharide (LPS) was established to study the effect of DEX on the expression of cell-related inflammatory factors. ADRA2A gene knockout THP-1 cells (THP-1^KO ) were constructed by CRISPR technology, and the effect of DEX on the expression of inflammatory factors of THP-1^KO cells was dete

SUBMITTER: Zhang B 

PROVIDER: S-EPMC10898205 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature