当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Dexmedetomidine inhibits apoptosis and expression of COX-2 induced by lipopolysaccharide in primary human alveolar epithelial type 2 cells.

Dexmedetomidine inhibits apoptosis and expression of COX-2 induced by lipopolysaccharide in primary human alveolar epithelial type 2 cells.

Abstract：

:Alveolar epithelial type II cells (ATII cells) are the main target cells being damaged and releasing the inflammatory mediators during acute respiratory distress syndrome (ARDS). Extensive apoptosis of epithelial cells leads to the breakdown of the alveolar-epithelial barrier in ARDS. Cyclooxygenase-2 (COX-2) plays an important role in pulmonary inflammatory response. Dexmedetomidine (DEX), a potent selective α2 adrenergic receptor (α2-AR) agonist, presents sedative, anxiolytic, and analgesic effects for anesthetic procedures. DEX has anti-apoptotic and anti-inflammatory properties. Our study demonstrated that DEX exerted anti-apoptotic effect on primary human epithelial cells with the inhibition of caspase activation, which was partly via the α2AR/PI3K/AKT pathway. Moreover, DEX significantly reduced the expression of COX-2 as well as prostaglandinE2 (PGE2) and tumor necrosis factor-α (TNF-α) production induced by lipopolysaccharide (LPS). Our next step is to determine whether DEX can regulate apoptosis in animal models. These results suggest DEX may be a promising therapy for preventing and treating ARDS as well as chronic diseases by directly targeting epithelial cell actions.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sun J,Zheng S,Yang N,Chen B,He G,Zhu T

doi

10.1016/j.bbrc.2019.07.023

subject

Has Abstract

pub_date

2019-09-10 00:00:00

pages

89-95

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)31359-2

journal_volume

517

pub_type

杂志文章

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