膜联蛋白A5可改善HO诱导的SH-SY5Y细胞的细胞毒性。

Annexin A5 ameliorates HO-induced cytotoxicity in SH-SY5Y cells.

作者信息

Mehdieh Marzieh, Rafiei Dehbidi Gholamreza, Morowvat Mohammad Hossein, Safari Fateme, Zare Farahnaz, Rastegari Banafshe, Takhshid Mohammad Ali

机构信息

Division of Medical Biotechnology, Department of Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.

Diagnostic Laboratory Sciences and Technology Research Center, Paramedical School, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Mol Biol Rep. 2025 Jun 29;52(1):653. doi: 10.1007/s11033-025-10726-6.

DOI:10.1007/s11033-025-10726-6

PMID:40581889

Abstract

BACKGROUND

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 HO-induced cell death, reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP) dissipation, and expression of Bax, Bcl2, and NRF2 in SH-SY5Y cells.

METHODS

SH-SY5Y cells were treated with different concentrations of HO, 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.

RESULTS

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

CONCLUSION

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

摘要

背景

氧化应激、线粒体功能障碍和细胞凋亡之间的复杂相互作用导致神经退行性疾病（ND）的发病机制。膜联蛋白A5（ANXA5）是一种钙结合多功能蛋白。本研究旨在评估ANXA5蛋白对HO诱导的SH-SY5Y细胞死亡、活性氧（ROS）积累、线粒体膜电位（MMP）耗散以及Bax、Bcl2和NRF2表达的可能保护作用。