Investigação da participação do sistema endocanabinóide e células da glia na dor muscular controlada pelo exercício físico

Abstract

Muscle pain affects approximately 11-24% of the population. It is of multifactorial origin, which may be caused by physical, emotional, psychological and social factors and is increasingly found in clinical practice. Studies have shown that physical exercise is an activity that helps to control pain. Cannabinoid receptor type 2 (CB2) expressed in peripheral tissues and inflammatory cells, appear to be involved in pain control. In addition, studies have shown that these receptors are also expressed in the central nervous system, including microglial cells. Thus, the present study investigated the participation of CB2 receptors and the involvement of the spinal microglia in the control of muscle pain by exercise. For this, were used C57BL/6 female mice, weighing between 20 and 25g. The nociceptive threshold was measured by Von Frey filaments test and hot plate test. The muscular pain model was induced by intramuscular injection of carrageenan in the right gastrocnemius muscle. To verify the levels of pro-inflammatory cytokines, we performed the ELISA assay. Muscle pain can lead to inflammation with increased local temperature, so we use thermography technique to check for changes in the local temperature of the animals. The following drugs were used, AM630, to investigate the involvement of CB2 receptors, MAFP to evaluate the role of endocannabinoids and minocycline to investigate the role of microglia. After the third week of swimming, the animals showed a reduction in mechanical allodynia and thermal hyperalgesia induced by carrageenan i.m. The AM630, reversed the antinociception induced by exercise in both nociceptive tests. MAFP inhibited muscle nociception in animal exercised only in the hot plate test. Minocycline blocked nociception only in the sedentary animals with muscular pain. The results of the ELISA assay showed that exercise reduced TNF-α levels, which were found in animals with increased muscle pain, which have not been exercised. Basaline levels of IL-1β showed reduced only in animals submitted to muscular pain model and underwent physical training. By thermographic analysis, we find a reduction in the local temperature of trained animals with muscular pain. Microglia appear to be involved in thermoregulation location of animal muscle pain exercised because when the microglia were blocked by minocycline, body temperature was increased in these animals. Thus, we conclude that exercise inhibits muscle pain induced by carrageenan, CB2 receptors participate in this pain control and microglia seems to be involved in the genesis and maintenance of muscle pain, with the release of pro-inflammatory cytokines.