الفهرس 
Benign prostatic hyperplasia:
Pathway signaling modulation by silymarin:Only 14 pages are availabe for public view
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Abstract
Benign prostatic hyperplasia (BPH) is considered a
normal part of the aging process in men and is characterized by an
imbalance between cell proliferation and apoptosis. Our study aimed to
investigate the potential protective role of silymarin (SIL) against
testosterone-induced BPH in rats and to elucidate the molecular
mechanisms underlying SIL pro-apoptotic and anti-proliferative effects.
Methods: Forty adult male Wistar rats were divided equally into four
groups: control group, BPH group (3 mg/kg testosterone propionate, s.c.
for 14 days, SIL group (50 mg/kg SIL, orally, once daily concomitantly
with 3 mg/kg testosterone propionate s.c.) and inhibitor group (50 mg/kg
SIL orally concomitantly with 3 mg/kg testosterone, s.c. and 0.5 mg/rat
Z-VAD-FMK, i.p.).
Results: Silymarin induced caspase-dependent apoptosis in BPH as SIL
significantly reduced prostatic Bcl-2 protein and increased Bax protein
concentration. Also, SIL downregulated survivin (Inhibitor of apoptosis
protein (IAPs) gene expression in rat prostate assisting mainly caspasedependent
pathway. Silymarin significantly decreased cytochrome-c
cytosolic concentration and increased caspase 3 activity compared to
BPH group. Silymarin significantly increased the content of p27/kip1
(Cyclin dependent kinase inhibitor (CDKIs) promoting cell cycle arrest.
The histological features of BPH such as hypertrophy, papillary
projections formation, improved in SIL group.
Conclusion: Silymarin showed a significant anti-proliferative and proapoptotic
role in BPH and accordingly it could be effectively and safely
used as a treatment tool in cases of BPH or prostatic disorders.