Seaweeds have attracted special interest as good sources of sulphated polysaccharides (SP) for use in pharmaceutical industries and biotechnology. In this study, we evaluated the effects of SP from the red seaweed Gracilaria cornea (Gc-TSP) in nociceptive and inflammatory models. In mice, Gc-TSP (3, 9 or 27 mg ⁄ kg) significantly reduced nociceptive responses, as measured by the number of writhes, at all tested doses. In a formalin test, Gc-TSP significantly reduced licking time in both phases of the test at a dose of 27 mg ⁄ kg. In a hot-plate test, the antinociceptive effect was observed only in animals treated with 27 mg ⁄ kg of Gc-TSP, suggesting that the analgesic effect occurs through a central action mechanism at the highest dose. Gc-TSP (3, 9 or 27 mg ⁄ kg) caused only a slight reduction in neutrophil migration in the rat peritoneal cavity. However, lower doses of Gc-TSP (3 and 9 mg ⁄ kg) significantly inhibited paw oedema induced by carrageenan, especially at 3 hr after treatment. Reduction in oedema was confirmed by myeloperoxidase activity in the affected paw tissue. In addition, treatment (s.c.) of animals with different doses of Gc-TSP inhibited paw oedema induced by dextran within the first hour in all doses tested. After 14 consecutive days of intraperitoneal administration of Gc-TSP (9 mg ⁄ kg), we measured the wet weight of the liver, kidney, heart, spleen and thymus and performed biochemical, haematological and histopathological evaluations. No systemic damage was found. These results indicate that Gc-TSP possesses analgesic and anti-inflammatory effects and is a potentially important tool worthy of further study.Inflammation is a protective response initiated after injury through physical damage or infection by microorganisms. Consisting of both systemic and local responses, inflammation is an essential biological process with the conserved functions of eliminating the noxious factors, promoting tissue repair and wound healing and establishing memory, which enables the host to mount a faster and more specific response upon a future encounter with the relevant stimulus [1]. Tissue damage, inflammation or injury to the nervous system may result in chronic neuropathic pain characterized by increased sensitivity to painful stimuli, the perception of innocuous stimuli as painful and spontaneous pain [2].A wide variety of noxious mechanical, thermal and chemical stimuli induce a marked inhibition in the activity of spinal dorsal horn convergent neurons, and it has been suggested that supra spinal neural system mediates this inhibition control through descending pathways. The sensitization of primary afferent nociceptors is common for all inflammatory pain types, leads to a state of hyperalgesia and ⁄ or allodynia in human beings and is well described as nociception in animal models [3].The administration of non-steroidal anti-inflammatory drugs is an important tool in the suppression of the inflammatory response in a clinical context and has the ability to inhibit initial or later manifest...