The aim of this study was to assess
cyclooxygenase (COX)-1 and COX-2 expression in skeletal muscle after an
ischemia-reperfusion (I/R). Male Sprague-Dawley rats were subjected to unilateral hindlimb
ischemia for 2 h and then euthanized after 0, 1, 2, 4, 6, 10, 24, and 72 h of reperfusion. The COX
protein and
mRNA were assessed in control and injured gastrocnemius muscle. Muscle damage was indirectly determined by plasma
creatine kinase activity and
edema by weighing wet muscle.
Creatine kinase activity in plasma increased as early as 1 h after reperfusion and returned to control levels by 72 h of reperfusion.
Edema was observed at 6 and 10 h of reperfusion, but histological investigations showed an absence of tissular inflammatory cell infiltration. COX-1
mRNA was expressed in control muscle and was increased at 72 h of reperfusion, but the levels of associated COX-1
protein detected in control and injured gastrocnemius muscle were similar. COX-2
mRNA was not, or only slightly, detectable in control muscle and after I/R. In contrast, I/R induced major overexpression of COX-2 immunoreactivity at 6 and 10 h of reperfusion with a maximum
at 10 h, whereas COX-2
protein was undetectable in control muscle. In conclusion, hindlimb I/R induced a large overexpression of COX-2 but not COX-1
protein between 6 and 10 h after injury. These results suggest a role for COX-2
enzyme in such pathophysiological conditions of the skeletal muscle.