%0 Journal Article
%T Antinociceptive and Antioxidant Activities of Phytol In Vivo and In Vitro Models
%A Camila Carolina de Menezes Patr¨ªcio Santos
%A Mirian Stiebbe Salvadori
%A Vanine Gomes Mota
%A Luciana Muratori Costa
%A Antonia Amanda Cardoso de Almeida
%A Guilherme Ant£¿nio Lopes de Oliveira
%A J¨¦ssica Pereira Costa
%A Dami£¿o Pergentino de Sousa
%A Rivelilson Mendes de Freitas
%A Reinaldo N¨®brega de Almeida
%J Neuroscience Journal
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/949452
%X The objective of the present study was to evaluate the antinociceptive effects of phytol using chemical and thermal models of nociception in mice and to assess its antioxidant effects in vitro. Phytol was administered intraperitoneally (i.p.) to mice at doses of 25, 50, 100, and 200£¿mg/kg. In the acetic acid-induced writhing test, phytol significantly reduced the number of contortions compared to the control group ( ). In the formalin test, phytol reduced significantly the amount of time spent in paw licking in both phases (the neurogenic and inflammatory phases), this effect being more pronounced in the second phase ( ). Phytol also provoked a significant increase in latency in the hot plate test. These antinociceptive effects did not impaire the motor performance, as shown in the rotarod test. Phytol demonstrated a strong antioxidant effect in vitro in its capacity to remove hydroxyl radicals and nitric oxide as well as to prevent the formation of thiobarbituric acid reactive substances (TBARS). Taken as a whole, these results show the pronounced antinociceptive effects of phytol in the nociception models used, both through its central and peripheral actions, but also its antioxidant properties demonstrated in the in vitro methods used. 1. Introduction The sensation of pain accompanies the majority of human diseases, alerting the body to the presence of harmful stimuli [1]. Pain may be modulated by a series of behavioral events, since, in addition to transmission of the stimulus that is causing the pain, the process also involves different emotional, environmental, and cognitive factors [2, 3]. Nociception involves activating sensorial neurons that transmit the nociceptive stimulus at spinal and supraspinal levels [4, 5]. Furthermore, following tissue damage, nociceptors are activated through the release of various mediators such as excitatory amino acids, protons, peptides, and cytokines that, in turn, act on specific receptors, activating various signaling cascades, which will result in the nociceptor membrane depolarization through the activation of second messengers or the sodium or calcium entry into the cell [3, 6¨C8]. Substances that are able to block these signal pathways, both at central and peripheral levels, represent important tools for pain control [9]. The current pharmacological treatment of pain consists in three main groups: central analgesics (opioids), peripheral analgesics (nonsteroidal antiinflammatory drugs-NSAIDs), and adjuvant drugs (antidepressants, anticonvulsants, and local anesthetics) [10, 11]. The development of new drugs
%U http://www.hindawi.com/journals/neuroscience/2013/949452/