MiR-27a-3p protects against NaAsO2-induced neuronal apoptosis in HT22 cells

被引：0

作者：

Qiyao Zhang ^{[1
]}

Siqi Zhao ^{[1
]}

Teng Ma ^{[1
]}

Yujie Wang ^{[1
]}

Shiqing Xu ^{[1
]}

Suhua Wang ^{[2
]}

Xiaohui Wang ^{[1
]}

Li Wang ^{[1
]}

机构：

[1] School of Public Health, Baotou Medical College, Inner Mongolia, Baotou

[2] Ulanqab Medical College, Inner Mongolia, Baotou

来源：

Scientific Reports | / 15卷 / 1期

基金：

中国国家自然科学基金;

关键词：

Apoptosis; Arsenic; Hippocampus; miR-27a-3p;

D O I：

10.1038/s41598-025-99195-2

中图分类号：

学科分类号：

摘要：

Environmental arsenic exposure is closely related to nerve damage. Recent research suggests miR-27a-3p is involved in the development of certain neurodegenerative and neuropsychiatric diseases. Nonetheless, the precise impact of miR-27a-3p on neuron functioning in the hippocampus remains unclear. In this investigation, models were established using NaAsO2-treated mice and cells to investigate this aspect. Male C57BL/6J mice were given drinking water containing sodium arsenite (0, 0.5, 5, or 50 ppm) for 48 weeks. The results showed that sodium arsenite induced apoptosis in mouse neurons. After 6 μmol/L sodium arsenite treatment in HT22 cells, miR-27a-3p expression level was decreased, FTO, DRP1 and p-DRP1 (Ser616), neuronal apoptosis and pro-apoptotic proteins (Bax and cleaved asparaginase 3) were increased, and anti-apoptosis proteins Bcl-2 and MMP were decreased, which indicated that sodium arsenite could activate FTO/DRP1 pathway. Furthermore the process could be reversed by miR-27a-3p mimics. This study demonstrates that miR-27a-3p alleviates sodium arsenite-induced mitochondrial dysfunction and apoptosis in HT22 cells by inhibiting the FTO/DRP1 pathway. This study provides a scientific basis for finding early biomarkers for the control of arsenic-induced neurotoxicity and discovering new prevention and control measures. © The Author(s) 2025.

引用

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