# Pulsatilla Saponin D Suppresses Proliferation and Induces Apoptosis in Human Prostatic Cells

**Authors:** Yuzhong Chen, Ping Zhou, Yangtao Jin, Dongyan Huang, Xin Su, Congcong Shao, Juan Jiang, Rongfu Yang, Jianhui Wu

PMC · DOI: 10.3390/cells14211706 · 2025-10-30

## TL;DR

Pulsatilla saponin D, a natural compound, may treat benign prostatic hyperplasia by reducing cell growth and inducing cell death in prostate cells.

## Contribution

This is the first study to show that Pulsatilla saponin D inhibits proliferation and induces apoptosis in prostatic cells linked to BPH.

## Key findings

- PSD significantly inhibits proliferation and induces apoptosis in human prostatic cells.
- PSD downregulates androgen receptor expression and modulates multiple signaling pathways.
- Transcriptome analysis and RT-qPCR confirm PSD's effects on key pathways like PI3K/AKT and TNF.

## Abstract

The growing global aging population is contributing to an increasing burden of benign prostatic hyperplasia (BPH), highlighting the need for novel, highly effective and low-toxicity therapies. In light of its well-documented anti-inflammatory and anti-tumor properties, we investigated the potential of the natural product Pulsatilla saponin D (PSD) in treating BPH. For the first time, we demonstrate that PSD significantly inhibits the proliferation of and induces apoptosis in the immortalized human normal prostatic stromal cell line, human prostate fibroblasts, and the human benign prostatic hyperplasia epithelial cell line. Mechanistic studies involving transcriptome analysis and RT-qPCR validation revealed that PSD likely exerts its effects by downregulating the expression of the androgen receptor and by modulating multiple signaling pathways synergistically, including the Phosphatidylinositol 3-kinase/Protein Kinase B, Tumor Necrosis Factor, Hypoxia-Inducible Factor-1 and Interleukin-17 pathways.

## Linked entities

- **Chemicals:** Pulsatilla saponin D (PubChem CID 11650910)
- **Diseases:** benign prostatic hyperplasia (MONDO:0010811)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PTK2B (protein tyrosine kinase 2 beta) [NCBI Gene 2185] {aka CADTK, CAKB, FADK2, FAK2, PKB, PTK}, PIK3R1 (phosphoinositide-3-kinase regulatory subunit 1) [NCBI Gene 5295] {aka AGM7, GRB1, IMD36, p85, p85-ALPHA, p85alpha}, AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}
- **Diseases:** tumor (MESH:D009369), inflammatory (MESH:D007249), toxicity (MESH:D064420), BPH (MESH:D011470)
- **Chemicals:** PSD (MESH:C000601508)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12610027/full.md

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Source: https://tomesphere.com/paper/PMC12610027