[Effect of hypoxia and IL-1beta on COX-2 expression and PGE2 release in human nasal epithelia]

Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2009 Feb;23(4):163-7.
[Article in Chinese]

Abstract

Objective: To detect cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human nasal epithelia (HNE) induced by hypoxia and/or IL-1beta of different time gradient, and to investigate their roles in nasal inflammatory pathogenesis.

Method: Western Blot and fluorescent real time quantitative PCR were performed to detect the expression of COX-2 in HNE induced by hypoxia and/or IL-1beta. The concentrations of PGE2 were determined by enzyme immunoassay. Median comparison was statistically treated by rank sum test, and generalized linear model was used to analyze the association of hypoxia with IL-1beta.

Result: Weak expressions of COX-2 and PGE2 were detected in normal HNE. COX-2 expression and PGE2 release increased in HNE induced by hypoxia and/or IL-1beta in time-dependent manner. Stronger expressions of COX-2 and PGE2 induced by hypoxia and/or IL-1beta than control were detected on different time (P < 0.05). The strongest inducible effect was found in hypoxia+IL-1beta group, and inducible effect decreased in hypoxia group and IL-1beta group in turn. The expressions of COX-2 and PGE2 in hypoxia+IL-1beta group were more than the sum of hypoxia group and IL-1beta group on same time.

Conclusion: Hypoxia and/or IL-1beta effectively induce COX-2 expression and PGE2 release in HNE. Synergistic effect between hypoxia and IL-1beta has been found in induction of COX-2 and PGE2 in HNE. Results indicate that the increased expressions of COX-2 and PGE2 are involved in inflammation of HNE induced by hypoxia and/or IL-1beta in vitro.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Hypoxia
  • Cells, Cultured
  • Cyclooxygenase 2 / metabolism*
  • Dinoprostone / metabolism*
  • Humans
  • Interleukin-1beta / pharmacology*
  • Nasal Mucosa / cytology
  • Nasal Mucosa / metabolism*

Substances

  • Interleukin-1beta
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Dinoprostone