RESUMEN
Peripheral neuropathies are common side effects of chemotherapeutic drugs, including taxanes, platinum-based drugs, vinca alkaloids, and thalidomide. The most common symptoms are numbness, tingling and/or burning pain in a stocking-glove distribution. Severe peripheral neuropathies result in dose reductions, a change in chemotherapy regimen, or early cessation of chemotherapy. There are no proven interventions to prevent or treat chemotherapy-induced peripheral neuropathy. We designed and built a unique magnetic stimulator to clarify the effects of magnetic stimulation in the mouse paclitaxel-induced peripheral neuropathic pain model. Magnetic stimulation significantly reversed paclitaxel-induced mechanical hyperalgesia. The analgesic efficacy of magnetic stimulation was inhibited by naloxone, a µ opioid receptor antagonist. These findings indicate that the analgesic effect of magnetic stimulation is likely to be mediated by the endogenous opioid system. Furthermore, a combination of magnetic stimulation and pregabalin, a Ca(2+) channel blocker, induced a potent combinational analgesic effect, suggesting that analgesic drug dose reduction might be possible. These findings indicate that there is a potential therapeutic utility for magnetic stimulation in pain relief.
Asunto(s)
Analgesia/métodos , Magnetoterapia/métodos , Neuralgia/inducido químicamente , Neuralgia/terapia , Paclitaxel/toxicidad , Analgésicos/uso terapéutico , Animales , Hiperalgesia/inducido químicamente , Hiperalgesia/terapia , Masculino , Ratones , Ratones Endogámicos ICR , Dimensión del Dolor/efectos de los fármacos , Dimensión del Dolor/métodos , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Enfermedades del Sistema Nervioso Periférico/fisiopatologíaRESUMEN
Studies on the immune regulation of osteoclasts in rheumatoid arthritis have promoted the new research field of 'osteoimmunology', which investigates the interplay between the skeletal and immune systems at the molecular level. Accumulating evidence lends support to the theory that bone destruction associated with rheumatoid arthritis is caused by the enhanced activity of osteoclasts, resulting from the activation of a unique helper T cell subset, 'Th17 cells'. Understanding the interaction between osteoclasts and the adaptive immune system in rheumatoid arthritis and the molecular mechanisms of Th17 development will lead to the development of potentially effective therapeutic strategies.