The role of poly(ADP-ribose) polymerase-1 inhibitor in carrageenan-induced lung inflammation in mice

Mol Immunol. 2015 Feb;63(2):394-405. doi: 10.1016/j.molimm.2014.09.009. Epub 2014 Oct 7.

Abstract

Increasing indication is unveiling a role for poly(ADP-ribose) polymerase (PARP)-1 in the regulation of inflammatory/immune responses. The aim of the present study was to determine the potential anti-inflammatory effects of PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ) to explore the role of PARP-1 inhibitor in a mouse model of carrageenan-induced lung inflammation. A single dose of 5-AIQ (1.5mg/kg) was administered intraperitoneally (i.p.) 1h before λ-carrageenan (Cg) administration. We assessed the effects of 5-AIQ treatment on CD25(+), GITR(+), CD25(+)GITR(+), IL-17(+) and Foxp3(+) cells which were investigated using flowcytometry in pleural exudates and heparinized blood. We also evaluated mRNA expressions of IL-6, TNF-α, IL-1β, IL-10, CD11a, l-selectin (CD62L), ICAM-1, MCP-1, iNOS and COX-2 in the lung tissue. We further examined the effects of 5-AIQ on the key mediators of inflammation, namely COX-2, STAT-3, NF-kB p65, PARP-1, IkB-α and IL-4 protein expression in the lung tissue using western blotting. The results illustrated that the numbers of T cell subsets, IL-17(+) cytokine levels were markedly increased and Foxp3(+) production decreased in the Cg group. Furthermore, Cg-induced up-regulation of adhesion molecules, pro-inflammatory mediators and chemokine expressions. Western blot analysis revealed an increased protein expressions of COX-2, STAT-3 NF-kB p65 and PARP-1 and decreased IkB-α and IL-4 in the Cg group. PARP-1 inhibitor via 5-AIQ treatment reverses the action significantly of all the previously mentioned effects. Moreover, histological examinations revealed anti-inflammatory effects of 5-AIQ, whereas Cg-group aggravated Cg-induced inflammation. Present findings demonstrate the potent anti-inflammatory action of the PARP-1 inhibitor in acute lung injury induced by carrageenan.

Keywords: Carrageenan; Inflammatory mediators; Lung tissue; PARP-1 inhibitor; Pleural exudate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrageenan
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Cytokines / genetics
  • Cytokines / metabolism
  • Enzyme Inhibitors / pharmacology
  • Enzyme Inhibitors / therapeutic use*
  • Female
  • Forkhead Transcription Factors / metabolism
  • Gene Expression Regulation / drug effects
  • Glucocorticoid-Induced TNFR-Related Protein / metabolism
  • Inflammation Mediators / metabolism
  • Interleukin-17 / biosynthesis
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Isoquinolines / pharmacology
  • Isoquinolines / therapeutic use*
  • Lipid Peroxidation / drug effects
  • Lipid Peroxidation / genetics
  • Mice, Inbred BALB C
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Pneumonia / drug therapy*
  • Pneumonia / enzymology*
  • Pneumonia / pathology
  • Poly(ADP-ribose) Polymerase Inhibitors*
  • Poly(ADP-ribose) Polymerases / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / metabolism

Substances

  • 5-aminoisoquinolinone
  • Cell Adhesion Molecules
  • Cytokines
  • Enzyme Inhibitors
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Glucocorticoid-Induced TNFR-Related Protein
  • Inflammation Mediators
  • Interleukin-17
  • Interleukin-2 Receptor alpha Subunit
  • Isoquinolines
  • Poly(ADP-ribose) Polymerase Inhibitors
  • RNA, Messenger
  • Tnfrsf18 protein, mouse
  • Carrageenan
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Poly(ADP-ribose) Polymerases