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Related Experiment Video

Updated: Jan 24, 2026

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
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Effects of Salidroside on Trabecular Meshwork Cell Extracellular Matrix Expression and Mouse Intraocular Pressure.

Yuchen Fan1,2,3, Li Guo4, Jiahong Wei3

  • 1Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

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Salidroside effectively reduces extracellular matrix buildup in human trabecular meshwork cells and lowers intraocular pressure (IOP) in a mouse model of glaucoma. This suggests salidroside as a potential new treatment for primary open-angle glaucoma (POAG).

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Pharmacology

Background:

  • Primary open-angle glaucoma (POAG) is linked to elevated intraocular pressure (IOP) caused by extracellular matrix (ECM) accumulation in the trabecular meshwork (TM).
  • Salidroside, a compound from Rhodiola rosea, is known to inhibit profibrotic pathways in various organs.

Purpose of the Study:

  • To investigate salidroside's effect on transforming growth factor-beta 2 (TGF-β2)-induced ECM expression in human TM cells.
  • To evaluate salidroside's efficacy in reducing TGF-β2-induced ocular hypertension in a mouse model.

Main Methods:

  • Human TM cells were treated with TGF-β2 and salidroside; ECM gene and protein expression were analyzed.
  • Mice received intravitreal TGF-β2 or control vectors and daily salidroside injections; IOP was measured using a rebound tonometer.

Main Results:

  • Salidroside significantly inhibited TGF-β2-induced expression of fibronectin, collagen type IV, and laminin in TM cells.
  • Daily salidroside treatment lowered TGF-β2-induced ocular hypertension in mice, without affecting IOP in control eyes.

Conclusions:

  • Salidroside effectively minimizes TGF-β2-induced ECM accumulation in human TM cells.
  • Salidroside reduces ocular hypertension in a mouse model, indicating its potential as a novel therapeutic agent for POAG.