# A Sulfated Polysaccharide from Gelidium crinale Suppresses Oxidative Stress and Epithelial–Mesenchymal Transition in Cultured Retinal Pigment Epithelial Cells

## TL;DR

A sulfated polysaccharide from a red algae protects retinal cells from oxidative stress and cell transformation, offering potential for treating dry AMD.

## Contribution

A novel sulfated polysaccharide from Gelidium crinale is shown to inhibit oxidative stress and EMT in retinal cells.

## Key findings

- GNP at 600 μg/mL significantly reduced ROS levels to control levels in RPE cells.
- GNP inhibited EMT markers like N-cadherin and Vimentin while increasing E-cadherin.
- GNP activated the Nrf2/HO-1 pathway to combat oxidative stress.

## Abstract

Age-related macular degeneration (AMD) progresses to vision-threatening dry and wet forms, with no effective dry AMD treatments available. The sulfated polysaccharide (GNP, 25.8 kDa) derived from Gelidium crinale exhibits diverse biological activities and represents a potential source of novel therapeutic agents. This study employed a hydrogen peroxide (H2O2)-induced oxidative stress and epithelial–mesenchymal transition (EMT) model in retinal pigment epithelial (RPE) cells to investigate GNP’s protective mechanisms against both oxidative damage and EMT. The results demonstrated that GNP effectively suppressed oxidative stress, with the 600 μg/mL dose significantly inhibiting excessive reactive oxygen species (ROS) generation to levels comparable to untreated controls. Concurrently, at concentrations of 200–600 μg/mL, GNP inhibited NF-κB signaling and increased the Bax/Bcl-2 ratio, effectively counteracting H2O2-induced oxidative damage and cell apoptosis. Furthermore, in H2O2-treated ARPE-19 cells, 600 μg/mL GNP significantly reduced the secretion of N-cadherin (N-cad), Vimentin (Vim), and α-smooth muscle actin (α-SMA), while increasing E-cadherin (E-cad) expression, consequently inhibiting cell migration. Mechanistically, GNP activated the Nrf2/HO-1 pathway, thereby mitigating oxidative stress. These findings suggest that GNP may serve as a potential therapeutic agent for dry AMD.