Not sure what you guys think of it, maybe someone who knows more can fill me in but basically, though the study was done on the prostate, doesnt this mean it possibly causes a total reduction in ARs ??
In this study:
Zhu W, Zhang JS, Young CY. Silymarin inhibits
function of the androgen receptor by reducing nuclear
localization of the receptor in the human prostate
cancer cell line LNCaP. Carcinogenesis 2001;22:
Silymarin was demonstrated to diminish nuclear androgen receptor levels...although the research was done on the prostate. Most of the Silymarin anti-androgen research is done on the prostate, which is the problem. I'm having trouble finding studies that look directly at skeletal muscle, but some coaches such as Poliquin have pulled their athletes off of it in place of N-Acetyl-Cysteine due to possible anti-androgen properties.
Another study:
Department of Biochemistry and Molecular Biology, Mayo Graduate School, Mayo Clinic/Foundation, Rochester, MN 55905, USA PMID: 11532861 [PubMed - indexed for MEDLINE]
A number of reports have shown that the polyphenolic flavonoid silymarin (SM) is an effective anticancer agent. Agents with novel mechanisms of blocking androgen receptor (AR) function may be useful for prostate cancer prevention and therapy.
Previous studies showed that silibinin (SB), the major active component of SM, could inhibit cell proliferation of a human prostate cancer cell line, LNCaP, by arresting the cell cycle at the G(1) phase without causing cell death. This study further delineates the potential molecular mechanism by which SM and SB exhibit antiproliferative effects on androgen-responsive prostate cancer cells by inhibiting function of the AR. We observed that SM and SB inhibited androgen-stimulated cell proliferation as well as androgen-stimulated secretion of both prostate-specific antigen (PSA) and human glandular kallikrein (hK2). Additionally, for the first time, we show that an immunophilin, FKBP51, is androgen regulated and that this up-regulation is suppressed by SM and SB. We further demonstrate that transactivation activity of the AR was diminished by SM and SB using gene transfer of PSA promoter and hK2 androgen-responsive element constructs. However, expression and steroid-binding ability of total AR were not affected by SM in western blotting and ligand-binding assays. Intriguingly, we found that nuclear AR levels are significantly reduced by SM and SB in the presence of androgens using western blotting assay and immunocytochemical staining. This study provides a new insight into how SM and SB negatively modulate androgen action in prostate cancer cells.
What do you guys think ?