DISCOREA VILLOSA - appr

DISCOREA VILLOSA (Diosgenina)

La Dioscorea Villosa, nota anche come igname selvatico o wild yam, è una pianta appartenente alla famiglia delle Dioscoreacee, originaria del Canada e dei Paesi del sud degli Stati Uniti. Le specie appartenenti al genere Dioscoreacee sono molto numerose (circa 600), e tutte caratterizzate dalla notevole presenza di sapogenine e per questo motivo sono state utilizzate dall’industria farmaceutica per l’emisintesi di steroidi.
La Diosgenina, il più importante princìpio attivo della Dioscorea, è quindi un importante precursore degli steroidi, presente in natura sotto forma del glicoside dioscina o di altri eterosidi che vengono poi idrolizzati in ambiente acido e per questo è stata da sempre utilizzata dall’industria farmaceutica come materia prima per la produzione di ormoni.
Le parti utilizzate per l’estrazione della droga sono le radici e i rizomi; la raccolta avviene nel periodo autunnale, prima della fioritura. I costituenti principali della dioscorea sono saponine (in particolar modo dioscina e diosgenina), fitosteroli e tannini.
Industrialmente la diosgenina ricavata dalla Dioscorea Villosa è largamente impiegata per la produzione sia diprogesterone che di DHEA.
Il DHEA (deidroepiandrosterone) è un ormone steroideo prodotto principalmente dalla corteccia surrenale, stimolata dall’ACTH, a sua volta prodotto dall’ipofisi. Piccole quantità di DHEA sono inoltre prodotte dai testicoli, dalle ovaie e dalle cellule gliali.
Il DHEA è uno dei precursori del testosterone; ricordiamo infatti che nell’organismo umano la sintesi degli steroidi avviene nel modo seguente: colesterolo –> pregnenolone –> DHEA –> androstenedione –> testosterone.
Il DHEA circola a livello ematico soprattutto come solfato (DHEA-S); nel plasma circa l’80% di questo solfato è legato alla albumina, il restante 20% invece è legato a lipoproteine. La quantità di DHEA contenuta nell’organismo umano è correlata all’età del soggetto. Dopo la nascita si assiste a una significativa diminuzione dei livelli plasmatici di DHEA, livelli che rimangono bassi per il primo quinquennio. A partire dai cinque anni i livelli tornano ad aumentare per raggiungere l’apice verso i venticinque anni; da questo momento in poi si assiste a una progressiva diminuzione della concentrazione di DHEA nell’organismo; tale diminuzione comincia a diventare rapida a partire dai quaranta anni. A ottant’anni di età, il livello non supera il 10% del massimo raggiunto a venticinque anni. A causa di questa diminuzione dei suoi livelli plasmatici con l’età, molti autori hanno supposto che il DHEA fosse fortemente coinvolto con i processi che regolano l’invecchiamento, tant’è che la somministrazione di DHEA è stata consigliata alla fine degli anni ’90 come metodo anti-invecchiamento. Il DHEA sembra essere coinvolto in numerose funzioni biologiche tra le quali ricordiamo la regolazione e la stimolazione delle funzioni sessuali, la produzione di mielina (la guaina che avvolge i nervi), l’attivazione dell’enzima G6PD che contribuisce alla riduzione delle cellule adipose etc. 

STUDI CLINICI

1) Diosgenin ameliorates palmitate-induced endothelial dysfunction and insulin resistance via blocking IKKβ and IRS-1 pathways. Kang Liua, Wenwen Zhaoa, Xuejiao Gaoa, Fang Huanga, Junping Koub,Baolin Liua
Abstract

  • Objective – We investigated whether diosgenin, a widely used steroidal sapogenin, exerted protection against palmitate (PA)-induced inflammation and insulin resistance in the endothelium.
  • Methods – Human umbilical vein endothelial cells (HUVECs) were pretreated with diosgenin for 30 min, and then incubated with 100 μmol/L PA for 30 min or 24 h with or without insulin. IKKβ, p65 phosphorylation, serine phosphorylation of insulin receptor substrate-1 (IRS-1) at S307, tyrosine phosphorylation of IRS-1, Akt and eNOS activation were determined by Western blot analysis. Levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), endothelin-1 (ET-1) and plasminogen activator inhibitor-1 (PAI-1) were measured with ELISA Kits. Intracellular nitric oxide (NO) was viewed with fluorescence microscopy. Effects of diosgenin on insulin-mediated vasodilation was investigated in the isolated rat aortic rings.
  • Results – Diosgenin significantly reduced PA-enhanced IKKβ and NF-κB phosphorylation with inhibition of TNF-α and IL-6 production in endothelial cells at the concentrations of 0.1, 1 and 10 μmol/L, well demonstrating its anti-inflammatory activity in an IKKβ/NF-κB-dependent fashion. Meanwhile, diosgenin attenuated PA-induced serine phosphorylation (S307) of IRS-1 and restored IRS-1 tyrosine phosphorylation in response to insulin. The beneficial modulation of serine/tyrosine phosphorylation of IRS-1 by diosgenin contributed to the improvement of insulin signaling along PI3K/Akt/eNOS pathways and thereby increased insulin-mediated NO production. Salicylate (5 mmol/L), an inhibitor of IKKβ, showed similar activities as diosgenin. Diosgenin also remarkably inhibited ET-1 and PAI-1 production in the endothelial cells, and markedly restored the loss of insulin-mediated vasodilation in the presence of PA.
  • Conclusion – The above-mentioned evidence suggests that diosgenin ameliorated endothelial dysfunction involved in insulin resistance through an IKKβ/IRS-1-dependent manner, shows potential application in the treatment for the cardiovascular diseases including atherosclerosis.

 

2)  Dehydroepiandrosterone in the treatment of erectile dysfunction: a prospective, double-blind, randomized, placebo-controlled study. Werner J Reiter, Armin Pycha, Georg Schatzl, Alexej Pokorny Doris M Gruber Johannes C Huber Michael Marberger
Abstract

  • Objectives – In 1994, the Massachusetts Male Aging Study presented an inverse correlation of the serum levels of dehydroepiandrosterone (DHEA) and the incidence of erectile dysfunction (ED). We evaluated the efficacy of DHEA replacement in the treatment of ED in a prospective, double-blind, randomized, placebo-controlled study.
  • Methods – The inclusion criteria included ED, normal physical and neurologic examinations, serum levels of testosterone, dihydrotestosterone, prolactin, and prostate-specific antigen (PSA) within the normal range, and a serum DHEA sulfate level below 1.5 μmol/L. Also all patients had a full erection after a pharmacologic erection test with 10 μg prostaglandin E1; pharmacocavernosography showed no visualization in corporeal venous structures. Forty patients from our impotence clinic were recruited and randomly divided into two groups of 20 patients each. Group 1 was treated with an oral dose of 50 mg DHEA and group 2 with a placebo one time a day for 6 months. The International Index of Erectile Function (IIEF), a 15-item questionnaire, was used to rate the success of this therapy.
  • Results – Therapy response was defined as the ability to achieve or maintain an erection sufficient for satisfactory sexual performance according to the National Institutes of Health Consensus Development Panel on Impotence. DHEA treatment was associated with higher mean scores for all five domains of the IIEF. There was no impact of DHEA treatment on the mean serum levels of PSA, prolactin, testosterone, the mean prostate volume, and the mean postvoid residual urine volume.
  • Conclusions – Our results suggest that oral DHEA treatment may be of benefit in the treatment of ED. Although our patient data base is too small to do relevant statistical analysis, we believe that our data show a biologically obvious trend that justifies further extended studies.

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Quanto proposto è ad esclusivo scopo informativo e non sostituisce il medico a cui bisogna rivolgersi per i problemi relativi alla salute.