期刊
NEUROSCIENCE BULLETIN
卷 37, 期 4, 页码 535-549出版社
SPRINGER
DOI: 10.1007/s12264-020-00620-5
关键词
Subarachnoid hemorrhage; Ferroptosis; Inflammation; Liproxstatin-1
资金
- National Key R&D Program of China [2018YFC1312600, 2018YFC1312603]
- National Science Foundation of China [81870910, 81870908]
- Natural Science Foundation of Zhejiang Province, China [LY18H090007]
- Scientific Research Fund of Zhejiang Provincial Education Department, China [Y201941838]
Ferroptosis has been shown to contribute to neuronal damage after SAH, while liproxstatin-1 protects neurons from injury by preserving mitochondrial functions and ameliorating lipid peroxidation. Additionally, liproxstatin-1 alleviates neurological deficits and brain edema, reduces neuronal cell death, and restores redox equilibrium after SAH.
Ferroptosis is a form of iron-dependent regulated cell death. Evidence of its existence and the effects of its inhibitors on subarachnoid hemorrhage (SAH) is still lacking. In the present study, we found that liproxstatin-1 protected HT22 cells against hemin-induced injury by protecting mitochondrial functions and ameliorating lipid peroxidation. In in vivo experiments, we demonstrated the presence of characteristic shrunken mitochondria in ipsilateral cortical neurons after SAH. Moreover, liproxstatin-1 attenuated the neurological deficits and brain edema, reduced neuronal cell death, and restored the redox equilibrium after SAH. The inhibition of ferroptosis by liproxstatin-1 was associated with the preservation of glutathione peroxidase 4 and the downregulation of acyl-CoA synthetase long-chain family member 4 as well as cyclooxygenase 2. In addition, liproxstatin-1 decreased the activation of microglia and the release of IL-6, IL-1 beta, and TNF-alpha. These data enhance our understanding of cell death after SAH and shed light on future preclinical studies.
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