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<p>Intracerebral hemorrhage (ICH) is a serious hemorrhagic stroke. Secondary nerve injury can cause nerve cell ferroptosis (FER), which promotes oxidative stress and inflammatory response and has been associated with poor prognosis in patients. Chrysin (CHR) has various bioactivities, such as antioxidative stress, anti-inflammatory, anti-FER, and neuroprotective effects. However, the role and mechanism of CHR in ICH remain undetermined. Therefore, this study established the rat ICH model using an autologous blood injection to investigate the brain tissue and hippocampal neuron morphological changes via hematoxylin–eosin staining, Nissl staining, and transmission electron microscopy. Furthermore, FER-related indicators were detected using a reagent kit and western blotting. Moreover, the Morris water maze test was carried out to assess the cognitive function of rats. The results indicated that CHR treatment significantly reduced FER, oxidative stress, inflammation, and nerve injury in the hippocampus of ICH rats and improved their cognitive function. In addition, ML385, the Nrf2 inhibitor, reversed the CHR-induced upregulation of the Nrf2/GPX4 signaling pathway and aggravated cognitive dysfunction in ICH rats. In conclusion, this study indicated that CHR inhibits FER by regulating the Nrf2/GPX4 signaling pathway to alleviate nerve injury and improve cognitive dysfunction in ICH rats. Therefore, CHR can be employed as a new strategy for treating ICH.</p>

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Chrysin Improves Cognitive Dysfunction in Rats with Intracerebral Hemorrhage by Regulating the Nrf2/GPX4 Pathway to Inhibit Ferroptosis

  • 期刊论文

  • 发表日期：

    2025年11月13日

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  • Dachuang Guo,
  • Zhe Shao,
  • Dayuan Liu,
  • Yong Guan,
  • Dongye Lian,
  • Jigao Feng,
  • Caicai Zhang,
  • Hao Peng

摘要

Intracerebral hemorrhage (ICH) is a serious hemorrhagic stroke. Secondary nerve injury can cause nerve cell ferroptosis (FER), which promotes oxidative stress and inflammatory response and has been associated with poor prognosis in patients. Chrysin (CHR) has various bioactivities, such as antioxidative stress, anti-inflammatory, anti-FER, and neuroprotective effects. However, the role and mechanism of CHR in ICH remain undetermined. Therefore, this study established the rat ICH model using an autologous blood injection to investigate the brain tissue and hippocampal neuron morphological changes via hematoxylin–eosin staining, Nissl staining, and transmission electron microscopy. Furthermore, FER-related indicators were detected using a reagent kit and western blotting. Moreover, the Morris water maze test was carried out to assess the cognitive function of rats. The results indicated that CHR treatment significantly reduced FER, oxidative stress, inflammation, and nerve injury in the hippocampus of ICH rats and improved their cognitive function. In addition, ML385, the Nrf2 inhibitor, reversed the CHR-induced upregulation of the Nrf2/GPX4 signaling pathway and aggravated cognitive dysfunction in ICH rats. In conclusion, this study indicated that CHR inhibits FER by regulating the Nrf2/GPX4 signaling pathway to alleviate nerve injury and improve cognitive dysfunction in ICH rats. Therefore, CHR can be employed as a new strategy for treating ICH.