# Protective Effects of Cord Blood Serum (CBS) on Retinal Pigment Epithelium (ARPE-19) and Retinal Photoreceptor-like (661W) Cell Line Viability Under In Vitro Oxidative Stress

## TL;DR

Cord blood serum protects retinal cells from oxidative stress by improving cell viability and preserving cell structure through BDNF-TrkB signaling.

## Contribution

This study demonstrates the neuroprotective potential of cord blood serum in retinal cells under oxidative stress via BDNF-TrkB signaling.

## Key findings

- CBS significantly improved cell viability in retinal cells under oxidative stress.
- CBS-H preserved epithelial integrity by increasing ZO-1 expression in ARPE-19 cells.
- CBS maintained mitochondrial function and enhanced TrkB phosphorylation in 661W cells.

## Abstract

Neuroprotection represents a promising approach for mitigating retinal degeneration. Cord blood serum (CBS), rich in trophic factors such as the brain-derived neurotrophic factor (BDNF), has shown therapeutic potential for ocular surface diseases; however, its role in retinal neuroprotection remains underexplored. This study evaluates the protective effects of CBS on retinal pigment epithelium (ARPE-19) and photoreceptor-like (661W) cells exposed to oxidative stress. Cells were cultured in media supplemented with fetal bovine serum (FBS) or CBS with either high (CBS-H) or low (CBS-L) BDNF content. Oxidative stress was induced using hydrogen peroxide (H2O2), and cell viability was measured via an MTS assay. ZO-1 expression was analyzed in ARPE-19 cells to assess tight junction integrity, while mitochondrial function in 661W cells was examined using MitoRed staining. TrkB receptor involvement was investigated using the inhibitor K252a and Western blot analysis. CBS significantly improved cell viability under oxidative conditions. CBS-H increased ZO-1 expression in ARPE-19 cells, indicating preserved epithelial integrity. In 661W cells, CBS maintained mitochondrial integrity and enhanced TrkB phosphorylation, while TrkB inhibition reduced its protective effect. These findings indicate that CBS confers neuroprotection through BDNF-TrkB signaling together with other trophic factors, supporting its potential as a multifactorial therapeutic strategy for retinal degeneration that deserves further exploration.