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Silibinin Prevents TGFβ-Induced EMT of RPE in Proliferative Vitreoretinopathy by Inhibiting Stat3 and Smad3

Xinqi Ma1,2, Yiyu Xie1,2, Yajun Gong1,2

  • 1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, China.

Investigative Ophthalmology & Visual Science
|October 31, 2023
PubMed
Abstract

Insights

Silibinin effectively inhibits retinal pigment epithelial cell transition and prevents proliferative vitreoretinopathy formation. This compound shows potential as a novel therapeutic agent for treating PVR by modulating key molecular pathways.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Pharmacology

Background:

  • Proliferative vitreoretinopathy (PVR) is a major cause of vision loss following retinal detachment.
  • Epithelial-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells plays a critical role in PVR pathogenesis.
  • Identifying novel therapeutic targets to inhibit RPE-EMT and PVR formation is crucial.

Purpose of the Study:

  • To investigate the effects of silibinin on RPE-EMT and PVR formation.
  • To elucidate the underlying molecular mechanisms of silibinin's action.
  • To evaluate silibinin as a potential therapeutic agent for PVR.

Main Methods:

  • In vitro studies using ARPE-19 cells to assess EMT markers, cell morphology, and migration.
  • In vivo PVR model in rats induced by intravitreal injection of RPE cells.
  • Quantitative PCR (qPCR), Western blot (WB), scratch, transwell, and RNA-sequencing (RNA-seq) analyses.
  • Assessment of Smad3 and Stat3 phosphorylation and nuclear translocation.

Main Results:

  • Silibinin dose-dependently inhibited TGFβ1-induced EMT and migration of RPE cells in vitro.
  • Silibinin significantly prevented proliferative membrane formation in a rat PVR model.
  • RNA-seq identified suppression of EMT and migration-related genes by silibinin.
  • Silibinin reduced TGFβ1-induced Smad3 and Stat3 phosphorylation and Smad3 nuclear translocation.

Conclusions:

  • Silibinin effectively inhibits RPE-EMT in vitro and PVR formation in vivo.
  • Silibinin acts by inhibiting Smad3 phosphorylation and nuclear translocation via Stat3 inhibition.
  • Silibinin demonstrates significant potential as a therapeutic strategy for PVR.

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