, pero un estudio de un centro prestigioso publicado en una revista científica importante siempre va bien... 
(aunque sea una muestra pequeña).La Universidad de Griffith australiana ha publicado este estudio en "Frontiers in Inmunology", que concluye que "El antagonista opioide NTX (Naltrexona) tiene el potencial de negar la función inhibitoria de los receptores opioides en TRPM3 en células NK de pacientes con EM / SFC, lo que resulta en la remodelación de las señales de calcio, lo que a su vez afectará las funciones celulares, lo que respalda la hipótesis de que NTX puede tener potencial de uso como tratamiento para ME / CFS. Nuestros resultados demuestran, por primera vez, y en base a la nueva electrofisiología de la pinza de parche, posibles intervenciones farmacoterapéuticas en EM / SFC.".
Copio aquí el abstract:
Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients
La naltrexona restaura la función potencial de los canales iónicos del receptor de iones de Melastatina 3 deteriorada en células asesinas naturales (NKC) de pacientes con Síndrome de Fatiga Crónica / Encefalomielitis Mialgica
Helene Cabanas 1,2,3*, Katsuhiko Muraki 3,4, Donald Staines 1,2,3 and Sonya Marshall-Gradisnik 1,2,31 School of Medical Science, Griffith University, Gold Coast, QLD, Australia
2 The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Gold Coast, QLD, Australia
3 Consortium Health International for Myalgic Encephalomyelitis, National Centre for Neuroimmunology and Emerging Diseases, Griffith University, Gold Coast, QLD, Australia
4 Laboratory of Cellular Pharmacology, School of Pharmacy, Aichi-Gakuin University, Nagoya, Japan
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a seriously long-term and debilitating illness of unknown cause hallmarked by chronic pain and fatigue, memory and concentration impairment, and inflammation. ME/CFS hypothesis involves impaired Transient receptor potential melastatin 3 (TRPM3) ion channel function, affecting calcium signaling and Natural killer (NK) cell functions. Currently, substances called opioids, agonists of mu (μ)-opioid receptors (μOR), are the strongest painkillers clinically available for people suffering from strong or long-lasting pain characteristic of ME/CFS. μOR have been reported to specifically inhibit TRPM3 and to be expressed in immune cells where they play an immunomodulatory and immunosuppressive role. Naltrexone hydrochloride (NTX) acts as an antagonist to the μOR thus negating the inhibitory function of this opioid receptor on TRPM3. Therefore, understanding the mechanism of action for NTX in regulating and modulating TRPM3 channel function in NK cells will provide important information for the development of effective therapeutic interventions for ME/CFS. Whole-cell patch-clamp technique was used to measure TRPM3 activity in Interleukin-2 (IL-2) stimulated and NTX-treated NK cells for 24 h on eight ME/CFS patients and 8 age- and sex-matched healthy controls, after modulation with a TRPM3-agonist, pregnenolone sulfate (PregS), NTX and a TRPM3-antagonist, ononetin. We confirmed impaired TRPM3 function in ME/CFS patients through electrophysiological investigations in IL-2 stimulated NK cells after modulation with PregS and ononetin. Importantly, TRPM3 channel activity was restored in IL-2 stimulated NK cells isolated from ME/CFS patients after incubation for 24 h with NTX. Moreover, we demonstrated that NTX does not act as an agonist by directly coupling on the TRPM3 ion channel gating.
The opioid antagonist NTX has the potential to negate the inhibitory function of opioid receptors on TRPM3 in NK cells from ME/CFS patients, resulting in calcium signals remodeling, which will in turn affect cell functions, supporting the hypothesis that NTX may have potential for use as a treatment for ME/CFS. Our results demonstrate, for the first time, and based on novel patch clamp electrophysiology, potential pharmaco-therapeutic interventions in ME/CFS.
Podéis leer el artículo completo aquí: https://www.frontiersin.org/articles/10 ... 02545/full
Como no estoy para traducir, os pego aquí enlace a la traducción automática del estudio completo:
https://translate.google.es/translate?h ... 545%2Ffull