1. Academic Validation
  2. CPI-1189 protects neuronal cells from oxygen glucose deprivation/re-oxygenation-induced oxidative injury and cell death

CPI-1189 protects neuronal cells from oxygen glucose deprivation/re-oxygenation-induced oxidative injury and cell death

  • Aging (Albany NY). 2021 Feb 17;13(5):6712-6723. doi: 10.18632/aging.202528.
Yong-Jun Li 1 Yueli Zhan 2 Chengrui Li 1 Jianhong Sun 3 Chengliang Yang 3
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Lianshui County People's Hospital, Lianshui, China.
  • 2 Anxi Maternal and Child Health Hospital, Anxi, China.
  • 3 Department of Anesthesiology, Affiliated Hospital of Yangzhou University, Yangzhou, China.
Abstract

Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) induces profound oxidative injury and neuronal cell death. It mimics ischemia-reperfusion neuronal injury. CPI-1189 is a novel tumor necrosis factor alpha-inhibiting compound with potential neuroprotective function. Here in SH-SY5Y neuronal cells and primary murine cortical neurons, CPI-1189 pretreatment potently inhibited OGDR-induced viability reduction and cell death. In OGDR-stimulated neuronal cells, p38 phosphorylation was blocked by CPI-1189. In addition, CPI-1189 alleviated OGDR-induced Reactive Oxygen Species production, lipid peroxidation, and glutathione consumption. OGDR-induced neuronal cell Apoptosis was also inhibited by CPI-1189 pretreatment. Furthermore, in SH-SY5Y cells and cortical neurons, CPI-1189 alleviated OGDR-induced programmed necrosis by inhibiting mitochondrial p53-cyclophilin D-adenine nucleotide translocase 1 association, mitochondrial depolarization, and Lactate Dehydrogenase release to the medium. In summary, CPI-1189 potently inhibited OGDR-induced oxidative injury and neuronal cell death.

Keywords

CPI-1189; neurons; oxidative injury; oxygen glucose deprivation/re-oxygenation; signaling.

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