Ecdiesteroides y su actividad farmacológica sobre el músculo esquelético / Ecdysteroids and their pharmacological activity on skeletal muscle

Introducción: Los ecdiesteroides presentan cualidades únicas dentro del reino vegetal y animal. Su similitud a esteroides endógenos de mamíferos les otorga actividad biológica sobre el tejido muscular esquelético. Sin embargo, su mecanismo de acción está por definirse en su totalidad. Método: Se realizó una revisión narrativa utilizando la evidencia científica más relevante. Se consultaron de las bases de datos Medline, Google Scholar, Scielo y Wiley, incluyéndose y excluyéndose trabajos acordes a los criterios del autor. Resultados: La actividad de los ecdiesteroides, principalmente de la Ecdisterona (Ec), podría deberse a la interacción con Mas, receptor acoplado a proteína-G transmembrana (GPCR), y la posterior activación del receptor de estrógenos β (ER β) no nuclear. Dicho mecanismo de acción induce la activación de la ruta alternativa del Sistema Renina-Angiotensina-Aldosterona (RAA) aboliendo los mecanismos de degradación muscular y, mediante la activación indirecta de Erβ, se suprime la expresión del gen de la miostatina. Esta actividad biológica pudiera conferir a los ecdiesteroides propiedades farmacológicas óptimas para impedir la degradación proteico-muscular, tales como la regeneración y reparación del tejido. Conclusiones: Ec ha demostrado poseer propiedades farmacológicas interesantes para el abordaje alternativo de patologías musculodegenerativas por sus efectos anticatabólicos. Aunque prosigue la investigación para su implementación en la clínica, esta siendo utilizada en la industria deportiva y en ensayos para el tratamiento de diferentes patologías. (AU)

Introduction: Ecdysteroids present unique qualities within the plant and animal kingdoms. Their similarity to en-dogenous mammalian steroids allows them to present biological activity on skeletal muscle tissue. However, this molecule’s action mechanism remains to be fully understood. Method: A narrative review was carried out using the most relevant scientific evidence. Different databases such as Medline, Google Scholar, Scielo and Wiley were consulted. Works were included or excluded according to the author ́s criterium. Results: Ecdysteroids’ activity, mostly that of ecdysterone, might be due to the interaction with Mas receptor, a transmembrane G-Protein Coupled Receptor (GPCR), and the subsequent indirect activation of β-Estrogen Recep-tor ́s (β-ER) non-nuclear form. Said action mechanism induces the alternative pathway activation of the Renin-An-giotensin-Aldosterone System (RAAS), abolishing muscular degradation mechanism. Finally, through β-ER activa-tion, the myostatin gene is supressed. This biological activity could provide ecdysteroids optimal pharmacological properties to prevent muscular protein degradation. These include tissue regeneration and repair. Conclusions: Due to its anticatabolic effects, Ec has shown great pharmacological properties that could make it work as an alternative treatment for degenerative muscle pathologies. Although investigations regarding Ec are still in progress, it has already been used by the sports’ industry and in several clinical trials that focus on the treatment of other diseases. (AU)

Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone.

SCOPE: The phytoectysteroid ecdysterone (Ecdy) was reported to stimulate protein synthesis and enhance physical performance. The aim of this study was to investigate underlying molecular mechanisms particularly the role of ER beta (ERß). RESULTS: In male rats, Ecdy treatment increased muscle fiber size, serum IGF-1 increased, and corticosteron and 17ß-estradiol (E2) decreased. In differentiated C2C12 myoblastoma cells, treatment with Ecdy, dihydrotestosterone, IGF-1 but also E2 results in hypertrophy. Hypertrophy induced by E2 and Ecdy could be antagonized with an antiestrogen but not by an antiandrogen. In HEK293 cells transfected with ER alpha (ERα) or ERß, Ecdy treatment transactivated a reporter gene. To elucidate the role of ERß in Ecdy-mediated muscle hypertrophy, C2C12 myotubes were treated with ERα (ALPHA) and ERß (BETA) selective ligands. Ecdy and BETA treatment but not ALPHA induced hypertrophy. The effect of Ecdy, E2, and BETA could be antagonized by an ERß-selective antagonist (ANTIBETA). In summary, our results indicate that ERß is involved in the mediation of the anabolic activity of the Ecdy. CONCLUSION: These findings provide new therapeutic perspectives for the treatment of muscle injuries, sarcopenia, and cachectic disease, but also imply that such a substance could be abused for doping purposes.

[Experience in using ecdisten in the treatment of hymenolepiasis].

The paper presents the results of clinical and parasitological studies in 22 patients with hymenolepiasis after treatment with ecdisten. The drug was used in a dose of 5 ml thrice a day during two weeks. It normalized all clinical symptoms in 8 patients and improved most of them in other patients. The results of helminthoovoscopy were interpreted in terms of clinical data. The parasitological efficacy of ecdisten is 36.4%. Its good tolerance, no contraindications, and easiness-to-use permit the drug to be recommended as a supplementary health-improving medication.