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Cao, Yang; Li, Yin; He, Chao; Yan, Feng; Li, Jian-Ru; Xu, Hang-Zhe; Zhuang, Jian-Feng; Zhou, Hang; Peng, Yu-Cong; Fu, Xiong-Jie; Lu, Xiao-Yang; Yao, Yuan; Wei, Yu-Yu; Tong, Yun; Zhou, Yi-Fu; Wang, Lin
Neuroscience Bulletin/Neuroscience bulletin, 04/2021, Letnik: 37, Številka: 4Journal Article
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-1β, and TNF-α. These data enhance our understanding of cell death after SAH and shed light on future preclinical studies.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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