Annexin A5 ameliorates H₂O₂-induced cytotoxicity in SH-SY5Y cells

A complex interplay between oxidative stress, mitochondrial dysfunction, and apoptosis contributes to the pathogenesis of neurodegenerative diseases (ND). Annexin A5 (ANXA5) is a calcium-binding multifunctional protein. This study aimed to evaluate the possible protective effects of ANXA5 protein against H₂O₂-induced cell death, reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP) dissipation, and expression of Bax, Bcl2, and NRF2 in SH-SY5Y cells.

SH-SY5Y cells were treated with different concentrations of H₂O₂, and cell viability was determined using an MTT assay. MMP dissipation and ROS accumulation were measured using rhodamine 123 and DCF-DA flow cytometry. The DNA fragmentation assay and real-time PCR were conducted to determine the effects of the treatments on genomic DNA damage and gene expression.

H₂O₂ reduced the viability of SH-SY5Y cells in a dose-dependent manner (IC₅₀ = 550µM). Moreover, H₂O₂ at the IC₅₀ concentration induced ROS accumulation, MMP loss, increased Bax expression, and reduced NRF2 expression in the SH-SY5Y cells. ANXA5 reversed the cytotoxic effects of H₂O₂ on the SH-SY5Y cell viability, ROS accumulation, MMP loss, and gene expression.

ANXA5 can protect the SH-SY5Y cells against H₂O₂-induced oxidative stress, apoptosis, and mitochondrial dysfunction.