Intracerebral haemorrhage (ICH) can be a catastrophic event; even if the initial stages of the pathology were well-managed, a number of patients experience varied residual neurological deficits following the insult. Ferroptosis is a recently identified type of cell demise which is tightly linked to the neurological impairment associated with ICH. In the current work, the prophylactic impact of scalp acupuncture (SA) therapy on autologous blood injection murine models of ICH was investigated in order to establish whether SA could mitigate the secondary damage arising following ICH by moderating ferroptosis. The pathophysiological mechanisms associated with this process were also explored. Ludmila Belayev tests were utilised for the characterisation of neurological damage. Haematoxylin–eosin staining was employed in order to determine the cerebral impact of the induced ICH. Malondialdehyde (MDA) and iron titres in peri-haemorrhagic cerebral tissues were appraised using purchased assay kits. Transmission electron microscopy delineated mitochondrial appearances within nerve cell bodies from the area of haemorrhage. Western blotting techniques were utilised to assay the degree of protein expression of NeuN, sequestosome 1 (p62), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1). The frequencies of Nrf2, GPX4 and FTH1 positive cells, respectively, were documented with immunohistochemical staining. The results demonstrated that therapy with SA after ICH mitigated MDA and iron sequestration, diminished the appearance of contracted mitochondria with increased outer mitochondrial membrane diameter within the nerve cell bodies, and suppressed neuronal ferroptosis. The pathways responsible for these effects may encompass amplified p62, Nrf2, GPX4 and FTH1 expression, together with decreased Keap1 expression. Application of SA reduced identified neurobehavioural abnormalities after ICH; no disparities were observed between the consequences of SA therapy and deferoxamine delivery. It can be surmised that intervention with SA enhanced recovery after ICH by triggering the antioxidant pathway, p62/Keap1/Nrf2, and causing FTH1 and GPX4 upregulation, factors that participate in diminishing excess iron and thus in mitigating lipid peroxidation insults arising from ferroptosis following ICH.

脑出血 (ICH) 可能是灾难性事件；即使病理学的初始阶段得到良好管理，许多患者在损伤后仍会出现不同的残余神经功能缺损。铁死亡是最近发现的一种细胞死亡类型，与 ICH 相关的神经损伤密切相关。在目前的工作中，研究了头皮针 (SA) 疗法对 ICH 自体血液注射小鼠模型的预防性影响，以确定 SA 是否可以通过减轻铁死亡来减轻 ICH 后引起的继发性损伤。还探索了与该过程相关的病理生理机制。Ludmila Belayev 测试用于表征神经损伤。采用苏木精-伊红染色以确定诱导的 ICH 对大脑的影响。使用购买的检测试剂盒评估出血周围脑组织中的丙二醛 (MDA) 和铁滴度。透射电子显微镜从出血区域描绘了神经细胞体内的线粒体外观。蛋白质印迹技术用于测定 NeuN、sequestosome 1 (p62)、核因子红细胞 2 相关因子 2 (Nrf2)、Kelch 样 ECH 相关蛋白 1 (Keap1)、谷胱甘肽过氧化物酶 4 (GPX4) 的蛋白质表达程度) 和铁蛋白重链 1 (FTH1)。Nrf2、GPX4 和 FTH1 阳性细胞的频率分别用免疫组织化学染色记录。结果表明，ICH 后用 SA 治疗减轻了 MDA 和铁螯合，随着神经细胞体内线粒体外膜直径的增加，减少了收缩线粒体的出现，并抑制了神经元铁死亡。造成这些影响的途径可能包括 p62、Nrf2、GPX4 和 FTH1 表达的扩增，以及 Keap1 表达的降低。SA 的应用减少了 ICH 后已识别的神经行为异常；在 SA 治疗和去铁胺给药的结果之间没有观察到差异。可以推测，SA 的干预通过触发抗氧化途径 p62/Keap1/Nrf2 并导致 FTH1 和 GPX4 上调，参与减少过量铁的因素，从而减轻 ICH 后铁死亡引起的脂质过氧化损伤，从而促进 ICH 后的恢复.