| Abstrakt: |
Benign prostatic hyperplasia (BPH) is an age-related disease and characterized by nonmalignant enlargement of the prostate gland. Currently, it's etiology remains unclear. A previous report showed that autophagy is decreased in the human BPH cell line (BPH-1) compared with the normal prostate cells (RWPE-1). The purpose of this study was to investigate whether cordycepin (3′-deoxyadenosine) could alleviate BPH through activating autophagy in BPH-1 cells. BPH-1 cells were treated 100 μM cordycepin for 48-h and BPH-related markers, such as androgen receptor (AR), 5-alpha reductase 2 (5AR-2), prostate-specific antigen (PSA), and apoptosis-related markers (Bax and BCL-2) were examined via RT-qPCR, cell proliferation rates were measured via MTT assay, cell cycle-related proteins (Cdk1 and Cyclin B1), pro-inflammatory cytokines (TNF-α and IL-1β), and autophagy flux were determined via immunoblot. Treatment with 100 μM of cordycepin significantly decreased on AR (~63%), 5AR-2 (~46%), and PSA (~68%) mRNA expression levels in BPH-1 cells (p < 0.05). Cordycepin significantly decreased cell proliferation rates (~29%), Cdk1 (~65%), Cyclin B1 (~43%), and both TNF-α (~55%) and IL-1β (~60%) protein levels in BPH-1 cells (p < 0.05). Cordycepin (100 μM) significantly enhanced autophagy flux in accordance with increased AMPK and decreased ribosomal protein S6 (mTOR substrate) phosphorylation. These positive effects of cordycepin appear to occur via AMPK-mTOR-dependent autophagy signaling mechanism. This study suggests that cordycepin is a potent autophagy activator and a promising agent for the treatment of BPH and other autophagy-impaired diseases. [ABSTRACT FROM AUTHOR] |
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