脑出血（ICH）是一种严重的出血性中风，可引起严重的继发性神经损伤。然而，其发病机制仍有待探索。目前的工作研究了谷胱甘肽 S-转移酶 omega 2 (GSTO2) 在 ICH 中的作用及其潜在机制。使用氯化血红素刺激人神经母细胞瘤细胞 (SK-N-SH) 以模拟 ICH 样损伤。通过蛋白质印迹分析法检测GSTO2和谷胱甘肽过氧化物酶4（GPX4）的蛋白表达水平。通过细胞计数试剂盒8测定法评估细胞活力。通过 5-乙炔基-2'-脱氧尿苷测定法研究细胞增殖。通过流式细胞术分析细胞凋亡。通过酶联免疫吸附测定对白介素 6 和肿瘤坏死因子 α 水平进行定量。采用 Fe2 比色测定试剂盒检测 Fe2 含量。使用细胞活性氧 (ROS) 检测试剂盒检测 ROS 水平。使用丙二醛含量测定试剂盒评估丙二醛（MDA）水平。使用 GSH 检测试剂盒对 GSH 水平进行定量。进行免疫共沉淀测定以确定 GSTO2 和 GPX4 之间的关联。血红素刺激抑制 SK-N-SH 细胞增殖并促进细胞凋亡、细胞炎症、铁死亡和氧化应激。与对照组相比，经氯高铁红素处理的 SK-N-SH 细胞中 GSTO2 表达下调。此外，异位GSTO2表达抵消了氯化血红素诱导的细胞增殖抑制作用以及对细胞凋亡、炎症、铁死亡和氧化应激的促进作用。此外，GSTO2 与 SK-N-SH 细胞中的 GPX4 相关。 GPX4 沉默减弱了 GSTO2 过表达诱导的对氯化血红素刺激的 SK-N-SH 细胞损伤的影响。 GSTO2 通过上调 ICH 中的 GPX4 表达来改善 SK-N-SH 细胞凋亡、炎症、铁死亡和氧化应激，为 ICH 提供治疗策略。© 2024 Wiley periodicals LLC。

Intracerebral hemorrhage (ICH) is a severe hemorrhagic stroke and induces severe secondary neurological injury. However, its pathogenesis remains to be explored. The present work investigates the role of glutathione S-transferase omega 2 (GSTO2) in ICH and the underlying mechanism. Human neuroblastoma cells (SK-N-SH) were stimulated using hemin to mimic ICH-like injury. Protein expression levels of GSTO2 and glutathione peroxidase 4 (GPX4) were detected by western blot analysis assay. Cell viability was assessed by cell counting kit-8 assay. Cell proliferation was investigated by 5-ethynyl-2'-deoxyuridine assay. Cell apoptosis was analyzed by flow cytometry. Interleukin-6 and tumor necrosis factor-α levels were quantified by enzyme-linked immunosorbent assays. Fe2+ colorimetric assay kit was used to detect Fe2+ level. A cellular reactive oxygen species (ROS) assay kit was used to detect ROS levels. Malondialdehyde (MDA) level was assessed using the MDA content assay kit. GSH level was quantified using the GSH assay kit. Co-immunoprecipitation assay was performed to identify the association between GSTO2 and GPX4. Hemin stimulation suppressed SK-N-SH cell proliferation and promoted cell apoptosis, cell inflammation, ferroptosis, and oxidative stress. GSTO2 expression was downregulated in hemin-treated SK-N-SH cells in comparison with the control group. In addition, ectopic GSTO2 expression counteracted hemin-induced inhibitory effect on cell proliferation and promoting effects on cell apoptosis, inflammation, ferroptosis, and oxidative stress. Moreover, GSTO2 was associated with GPX4 in SK-N-SH cells. GPX4 silencing attenuated GSTO2 overexpression-induced effects on hemin-stimulated SK-N-SH cell injury. GSTO2 ameliorated SK-N-SH cell apoptosis, inflammation, ferroptosis, and oxidative stress by upregulating GPX4 expression in ICH, providing a therapeutic strategy for ICH.© 2024 Wiley Periodicals LLC.