Abstract
We have recently reported that intraperitoneal (i.p.) injection of thymulin at low doses (50 ng) resulted in thermal and mechanical hyperalgesia and upregulation of the level of interleukin-1β in the liver. In this study, we demonstrate that such injections of thymulin result in a significant elevation in the levels of TNF-α ( P<0.01), NGF ( P<0.01) and PGE 2 ( P<0.01) in the liver of the treated rats, in addition to the increase in the levels of IL-1β. Pretreatment with specific antagonists to each of these factors (polyclonal anti-TNF-α, anti-NGF antiserum and IL-1 receptor antagonist) did not result in the abolition of the hyperalgesia as assessed by the paw pressure, hot plate, paw immersion and tail flick tests. However, pretreatment with a combination of the above antagonist and antisera almost completely prevented thymulin-induced hyperalgesia. The cyclooxygenase inhibitor, meloxicam, reversed in a dose dependent manner (0.2, 0.4 and 2 mg/kg) thymulin effects as assessed by the different pain tests. It also abolished the thymulin-induced increase in the level of cytokines and NGF in the liver. Our results indicate that PGE 2 could be the key mediator of the hyperalgesic action of thymulin and the observed upregulation of proinflammatory cytokines and NGF.
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