[Effect of aging on pulmonary ICAM-1 and MCP-1 expressions in rats with lipopolysaccharide- induced acute lung injury]

Nan Fang Yi Ke Da Xue Xue Bao. 2010 Mar;30(3):584-7.
[Article in Chinese]

Abstract

Objective: To investigate the effect of aging on the expressions of monocyte chemoattractant protein 1 (MCP-1) and intercellular adhesion molecule 1 (ICAM-1) in the lung tissue of rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI).

Methods: Both young (3 months old) and aged (27 months old) female Wistar rats were randomly divided into two groups (n=8), namely the normal control and LPS-induced ALI groups. Immunohistochemistry for of ED-1 was used to detect the infiltrating inflammatory cells. Western blot and Northern blot analyses were employed for evaluating the expressions of MCP-1 and ICAM-1 at the protein and mRNA levels.

Results: Virtually no ED-1-positive cells were found in the lung tissue of the control rats in the young and aged groups. After LPS-induced ALI, ED-1-positive cells in the lung tissues increased significantly in both young and aged groups (P<0.05), and the increment was more obviously in the aged group (P<0.05). In the two normal control groups, the aged rats showed significantly higher expressions of MCP-1 and ICAM-1 than the young rats (P<0.05); LPS significantly up-regulated their expression in the young and aged groups (P<0.05), but the latter showed greater increments (P<0.05). The aged rats with ALI also showed significantly greater MCP-1 and ICAM-1 increments than those of the young rats (P<0.05).

Conclusions: Aging may upregulate lung MCP-1 and ICAM-1 expressions and enhance LPS-induced increments of MCP-1 and ICAM-1 expressions to exacerbate the pulmonary inflammation in rats.

Publication types

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

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / metabolism*
  • Aging*
  • Animals
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism*
  • Female
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism*
  • Lipopolysaccharides
  • Lung / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Up-Regulation

Substances

  • Chemokine CCL2
  • Lipopolysaccharides
  • RNA, Messenger
  • Intercellular Adhesion Molecule-1