Resveratrol Enhances Apoptosis in Endometriotic Stromal Cells

Ayumi Taguchi1, Kaori Koga1, Kei Kawana1

  • 1Department of Obstetrics and Gynecology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.

Abstract

Insights

Resveratrol (RVT) does not induce apoptosis in human endometriotic stromal cells (ESCs) alone but enhances TRAIL-induced apoptosis by suppressing survivin expression. This finding suggests RVT as a potential therapeutic agent for endometriosis.

Area of Science:

  • Reproductive biology
  • Cellular biology
  • Molecular medicine

Background:

  • Endometriosis pathogenesis involves resistance to apoptosis, inflammation, and invasion.
  • Resveratrol (RVT) is known to induce apoptosis in cancer cells, but its effect on endometriosis is unclear.
  • Targeting apoptosis in endometriotic stromal cells (ESCs) is a promising therapeutic strategy.

Purpose of the Study:

  • To investigate the effect of resveratrol (RVT) on apoptosis in human endometriotic stromal cells (ESCs).
  • To determine if RVT can induce or enhance apoptosis in ESCs, potentially as a treatment for endometriosis.

Main Methods:

  • Endometriotic tissues were collected from women with ovarian endometriosis.
  • Endometriotic stromal cells (ESCs) were isolated, cultured, and treated with RVT.
  • Apoptosis was assessed using annexin V-PI staining, and survivin mRNA expression was measured by RT-PCR.
  • ESCs were pre-treated with RVT and then exposed to TNF-α-related apoptosis-inducing ligand (TRAIL).

Main Results:

  • Resveratrol (RVT) alone did not induce apoptosis in ESCs.
  • RVT significantly reduced survivin mRNA expression in ESCs (P < 0.05).
  • Pre-treatment with RVT significantly enhanced TRAIL-induced apoptosis in ESCs (from 8.13% to 29.19%, P < 0.05).

Conclusions:

  • Resveratrol (RVT) suppresses survivin expression in human endometriotic stromal cells (ESCs).
  • RVT enhances TRAIL-induced apoptosis in ESCs, indicating a potential therapeutic role.
  • These findings suggest RVT as a potential agent for managing endometriosis by promoting apoptosis.