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<p>Subarachnoid hemorrhage (SAH) can cause severe neuronal damage and trigger multiple molecular mechanisms of cell death, among which ferroptosis has garnered significant attention due to its dependence on lipid peroxidation. In this study, ferroptosis-related markers were found to be significantly dysregulated in an in vitro SAH model, confirming the neuronal ferroptosis after SAH. Transcriptomic sequencing results indicated a marked downregulation of stearoyl-CoA desaturase 1 (SCD1), which was further validated by Western blot. Immunofluorescence demonstrated its colocalization with the neuronal marker NeuN. Overexpression of SCD1 effectively reduced ferroptosis-related markers and mitigated intracellular lipid accumulation. Additionally, supplementation with oleic acid (OA) which was the main product of SCD1, significantly alleviated hemoglobin (Hb)-induced ferroptosis. Furthermore, the ratio of saturated fatty acids (stearic acid, SA) to unsaturated fatty acids (OA) had a significant impact on neuronal survival. When the proportion of OA was increased (SA:OA = 1:2), ferroptosis was markedly inhibited. In conclusion, this study revealed the role and mechanism by which SCD1 affected neuronal ferroptosis by regulating oleic acid metabolism after SAH, providing a new potential target for mitigating neural injury after SAH.</p>

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SCD1-Mediated Lipid Metabolism Alleviates Neuronal Ferroptosis in Subarachnoid Hemorrhage: Role of Oleic Acid Supplementation

  • 期刊论文

  • 发表日期：

    2025年5月8日

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  • Jingyuan Zhou,
  • Fangbo Hu,
  • Taotao Hu,
  • Yikun Zhao,
  • Yunsong Pan,
  • Yong Sun,
  • Xiangxin Chen

摘要

Subarachnoid hemorrhage (SAH) can cause severe neuronal damage and trigger multiple molecular mechanisms of cell death, among which ferroptosis has garnered significant attention due to its dependence on lipid peroxidation. In this study, ferroptosis-related markers were found to be significantly dysregulated in an in vitro SAH model, confirming the neuronal ferroptosis after SAH. Transcriptomic sequencing results indicated a marked downregulation of stearoyl-CoA desaturase 1 (SCD1), which was further validated by Western blot. Immunofluorescence demonstrated its colocalization with the neuronal marker NeuN. Overexpression of SCD1 effectively reduced ferroptosis-related markers and mitigated intracellular lipid accumulation. Additionally, supplementation with oleic acid (OA) which was the main product of SCD1, significantly alleviated hemoglobin (Hb)-induced ferroptosis. Furthermore, the ratio of saturated fatty acids (stearic acid, SA) to unsaturated fatty acids (OA) had a significant impact on neuronal survival. When the proportion of OA was increased (SA:OA = 1:2), ferroptosis was markedly inhibited. In conclusion, this study revealed the role and mechanism by which SCD1 affected neuronal ferroptosis by regulating oleic acid metabolism after SAH, providing a new potential target for mitigating neural injury after SAH.