Rho-kinase signalling regulates CXC chemokine formation and leukocyte recruitment in colonic ischemia-reperfusion

Int J Colorectal Dis. 2010 Sep;25(9):1063-70. doi: 10.1007/s00384-010-0997-3. Epub 2010 Jul 1.

Abstract

Background and aims: Leukocyte recruitment is a key feature in ischemia-reperfusion (I/R)-induced tissue injury. The aim of the present study was to investigate the effect of Rho-kinase inhibition on I/R-provoked leukocyte recruitment in the colon.

Methods: C57BL/6 mice were subjected to 30 min of ischemia by clamping of the superior mesenteric artery followed by 120 min of reperfusion. Intraperitoneal pretreatment with the selective Rho-kinase inhibitors fasudil (4-40 mg/kg) and Y-27632 (1-10 mg/kg) was administered prior to induction of colonic I/R. Leukocyte-endothelium interactions were analyzed by intravital fluorescence microscopy. Colonic content of tumour necrosis factor-alpha (TNF-alpha) and the CXC chemokines macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC) were determined by ELISA. Additionally, colonic activity of myeloperoxidase (MPO), a marker of leukocyte infiltration, and malondialdehyde (MDA), were quantified.

Results: Fasudil and Y-27632 pretreatment decreased I/R-induced leukocyte rolling and adhesion by 76% and 96%, respectively. Moreover, Rho-kinase interference reduced formation of TNF-alpha, MIP-2 and KC by more than 68% in the reperfused colon. Additionally, the reperfusion-provoked increase in the levels of MPO and MDA in the colon decreased after Rho-kinase inhibition by 69% and 42%, respectively.

Conclusions: Our data demonstrate that inhibition of Rho-kinase activity decrease I/R-induced leukocyte rolling, adhesion and recruitment in the colon. Moreover, these findings show that Rho-kinase signalling regulates TNF-alpha and CXC chemokine formation as well as lipid peroxidation in the reperfused colon. Thus, targeting Rho-kinase signalling may be a useful strategy in order to protect against pathological inflammation in the colon.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Adhesion / drug effects
  • Cell Movement* / drug effects
  • Chemokine CXCL1 / biosynthesis
  • Chemokine CXCL1 / metabolism
  • Chemokine CXCL2 / biosynthesis
  • Chemokines, CXC / biosynthesis*
  • Colon / drug effects
  • Colon / enzymology
  • Colon / pathology*
  • E-Selectin / metabolism
  • Hemodynamics / drug effects
  • Leukocyte Count
  • Leukocyte Rolling / drug effects
  • Leukocytes / cytology*
  • Leukocytes / drug effects
  • Leukocytes / enzymology
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred C57BL
  • P-Selectin / metabolism
  • Peroxidase / metabolism
  • Protein Kinase Inhibitors / pharmacology
  • Reperfusion Injury / blood
  • Reperfusion Injury / enzymology*
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology
  • Signal Transduction* / drug effects
  • Tumor Necrosis Factor-alpha / metabolism
  • rho-Associated Kinases / antagonists & inhibitors
  • rho-Associated Kinases / metabolism*

Substances

  • Chemokine CXCL1
  • Chemokine CXCL2
  • Chemokines, CXC
  • Cxcl1 protein, mouse
  • E-Selectin
  • P-Selectin
  • Protein Kinase Inhibitors
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Peroxidase
  • rho-Associated Kinases