Related Experiment Video
Updated: Apr 30, 2026
Murine Prostate Micro-dissection and Surgical Castration
Published on: May 11, 2016
Antiangiogenic and finasteride therapies: responses of the prostate microenvironment in elderly mice
Larissa Akemi Kido1, Amanda Cia Hetzl1, Eduardo Marcelo Cândido1
1Department of Structural and Functional Biology, Institute of Biology, State University of Campinas (UNICAMP), Campinas, São Paulo, Brazil.
Aims:
The aim of this study was to evaluate the structural and molecular effects of antiangiogenic therapies and finasteride on the ventral prostate of senile mice.
Main Methods:
90 male FVB mice were divided into: Young (18 weeks old) and senile (52 weeks old) groups; finasteride group: finasteride (20mg/kg); SU5416 group: SU5416 (6 mg/kg); TNP-470 group: TNP-470 (15 mg/kg,) and SU5416+TNP-470 group: similar to the SU5416 and TNP-470 groups. After 21 days, prostate ventral lobes were collected for morphological, immunohistochemical and Western blotting analyses.
Key Findings:
The results demonstrated atrophy, occasional proliferative lesions and inflammatory cells in the prostate during senescence, which were interrupted and/or blocked by treatment with antiangiogenic drugs and finasteride. Decreased AR and endostatin reactivities, and an increase for ER-α, ER-β and VEGF, were seen in the senile group. Decreased VEGF and ER-α reactivities and increased ER-β reactivity were verified in the finasteride, SU5416 groups and especially in SU5416+TNP-470 group. The TNP-470 group showed reduced AR and ER-β protein levels.
Significance:
The senescence favored the occurrence of structural and/or molecular alterations suggesting the onset of malignant lesions, due to the imbalance in the signaling between the epithelium and stroma. The SU5416+TNP-470 treatment was more effective in maintaining the structural, hormonal and angiogenic factor balance in the prostate during senescence, highlighting the signaling of antiproliferation via ER-β.
Insights
Senescence promotes prostate changes, but antiangiogenic drugs and finasteride treatments can block these alterations. Combined SU5416 and TNP-470 therapy effectively balanced prostate structure and signaling in aging mice.
Area of Science:
- Urology
- Oncology
- Endocrinology
- Aging Research
Background:
- Senescence is associated with prostate structural and molecular alterations, potentially indicating early malignant changes.
- Hormonal and angiogenic signaling imbalances between prostate epithelium and stroma contribute to age-related prostate issues.
Purpose of the Study:
- To investigate the effects of antiangiogenic therapies (SU5416, TNP-470) and finasteride on the ventral prostate of senile mice.
- To evaluate the structural and molecular changes in the aging prostate and the impact of therapeutic interventions.
Main Methods:
- 90 male FVB mice were divided into young and senile groups.
- Senile mice received finasteride, SU5416, TNP-470, or a combination of SU5416+TNP-470 for 21 days.
- Prostate ventral lobes underwent morphological, immunohistochemical, and Western blotting analyses.
Main Results:
- Senescence induced prostate atrophy, lesions, and inflammation, which were mitigated by treatments.
- Treatments altered androgen receptor (AR), estrogen receptor (ER-α, ER-β), and vascular endothelial growth factor (VEGF) expression.
- The SU5416+TNP-470 combination showed the most significant impact on restoring hormonal and angiogenic balance.
Conclusions:
- Prostate senescence creates an environment conducive to malignant lesion development due to epithelial-stromal signaling imbalance.
- Combined SU5416 and TNP-470 therapy effectively maintained prostate structural, hormonal, and angiogenic balance in senile mice.
- The study highlights the antiproliferative signaling role of ER-β in maintaining prostate health during aging.
