Resveratrol induces apoptosis of benign prostatic hyperplasia epithelial cell line (BPH-1) through p38 MAPK-FOXO3a...

Area of Science:

• Biochemistry
• Cell Biology
• Molecular Medicine

Background:

• Resveratrol is known to inhibit prostate growth, a key feature of benign prostatic hyperplasia (BPH).
• The precise molecular mechanisms underlying resveratrol's effects on BPH remain largely unelucidated.
• Understanding these mechanisms is crucial for developing targeted therapeutic strategies for BPH.

Purpose of the Study:

• To investigate the effects of resveratrol on BPH epithelial cells.
• To elucidate the probable molecular mechanism through which resveratrol impacts BPH.
• To identify key signaling pathways and cellular processes involved.

Main Methods:

• Utilized the BPH-1 epithelial cell line for experimental treatments.
• Assessed cell viability, apoptosis, reactive oxygen species (ROS) accumulation, and cell cycle progression.
• Employed Western blot to analyze p38 MAPK activation and protein levels of FOXO3a, Bcl2, Bcl-XL, and caspase3.
• Investigated the roles of p38 MAPK and ROS by co-treatment with SB203580 (inhibitor) and N-Acetyl-L-cysteine (NAC, scavenger).

Main Results:

• Resveratrol significantly inhibited BPH-1 cell growth and induced apoptosis.
• Elevated levels of phosphorylated p38 MAPK and repressed FOXO3a were observed post-resveratrol treatment.
• Concomitant accumulation of ROS was detected, which was attenuated by SB203580 or NAC.
• Resveratrol treatment led to cell cycle arrest at the S phase.

Conclusions:

• Resveratrol activates the p38 MAPK pathway and represses FOXO3a in BPH-1 cells.
• This activation/repression cascade results in the downregulation of SOD2 and catalase, leading to increased ROS accumulation.
• The elevated ROS levels trigger apoptosis in BPH-1 cells, highlighting a key mechanism of resveratrol's anti-BPH effects.