Cyclooxygenase‐2 (Cox‐2) in injured human nerve and a rat model of nerve injury

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<jats:p><jats:bold>Abstract </jats:bold> Inflammation associated with nerve injury produces a number of pathogenic chemical mediators of which prostanoids are a potent component. Cyclooxygenases (Cox‐1 and Cox‐2) are the enzymes responsible for prostanoid production. We have investigated Cox‐2 immunoreactivity (Cox‐2‐IR) and glial activation in human injured (<jats:italic>n</jats:italic> = 16) and uninjured (<jats:italic>n</jats:italic> = 8) nerves and in the chronic constriction injury (CCI) model of nerve injury in the rat, using immunohistological and autoradiographic methods. Tissues were immunostained with antibodies to Cox‐2, CD‐68 (human macrophage marker), OX42 (rat microglial marker), or incubated with tritiated PK11195 (marker of glial activation), prior to image analysis. In human nerves, Cox‐2‐IR was detected in cells with morphology and distribution similar to macrophages/microglia – these were increased significantly in human nerve proximal to injury (p < 0.002), reaching a peak at 4–6 weeks after injury. In the rat CCI model, at 40 days after injury, microglia‐like cells with Cox‐2‐IR were increased significantly in the injured nerve (p < 0.004) and ipsilateral dorsal spinal cord (p < 0.008). PK11195‐binding results were similar for Cox‐2‐IR in chronic injured human nerve and rat tissues. These findings suggest that Cox‐2‐immunoreactive cells could play a role in processes associated with Wallerian degeneration, nerve regeneration, and the development of persistent pain. Selection of patients 4–6 weeks after nerve injury would be more likely to show any efficacy of Cox‐2 inhibitors.</jats:p>

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