Effect of aspirin and acetaminophen on proinflammatory cytokine-induced pain behavior in mice

Aspirin (ASA) is a widely used oral analgesic which acts as an inhibitor of cyclooxygenase. Acetaminophen (ACET) is also an effective analgesic and may selectively inhibit brain prostaglandin synthetase. Various proinflammatory cytokines injected into the central nervous system show pain behavior. In the present study, the effects of orally administered ASA and ACET on pain behaviors induced by various proinflammatory cytokines were examined. At a dose of 100 mg/kg, ASA or ACET did not affect the pain behavior induced by TNF-alpha (100 pg), IL-1beta (100 pg) or IFN-gamma (100 pg) administered intrathecally. However, at doses of 200 and 300 mg/kg, ASA or ACET significantly and dose-dependently attenuated pain behavior induced by TNF-alpha, IL-1beta or IFN-gamma administered intrathecally. Our results suggest that orally administered ASA and ACET produce antinociception by inhibiting the nociceptive action of TNF-alpha, IL-1beta or IFN-gamma administered intrathecally.