Neuroprotection by LY341122, a novel inhibitor of lipid peroxidation, against focal ischemic brain damage in rats.

@article{Huh2000NeuroprotectionBL,
  title={Neuroprotection by LY341122, a novel inhibitor of lipid peroxidation, against focal ischemic brain damage in rats.},
  author={Pil Woo Huh and Ludmila Belayev and W. Zhao and James A. Clemens and Jill Ann Panetta and Raul Busto and Myron D. Ginsberg},
  journal={European journal of pharmacology},
  year={2000},
  volume={389 1},
  pages={
          79-88
        }
}
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TLDR
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Early treatment with a novel inhibitor of lipid peroxidation (LY341122) improves histopathological outcome after moderate fluid percussion brain injury in rats.
TLDR
The hypothesis that lipid peroxidation and reactive oxygen species participate in the acute pathogenesis of TBI is reinforced, as treatment delayed until 3 hours after TBI did not provide significant histopathological protection.
Postischemic application of lipid peroxidation inhibitor U-101033E reduces neuronal damage after global cerebral ischemia in rats.
TLDR
The results indicate that free radical-induced lipid peroxidation contributes to reperfusion injury, a process that can be inhibited by antioxidants such as U-101033E.
Pyrrolopyrimidines: novel brain-penetrating antioxidants with neuroprotective activity in brain injury and ischemia models.
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The results suggest that antioxidant compounds with improved brain parenchymal penetration are better able to limit certain types of ischemic brain damage than those which are localized in the cerebral microvasculature.
Superior neuroprotective efficacy of a novel antioxidant (U-101033E) with improved blood-brain barrier permeability in focal cerebral ischemia.
TLDR
For treatment of transient focal ischemia, an antioxidant that crosses the blood-brain barrier might be superior to agents that predominantly act on the endothelium of the cerebral microvasculature.
Dimethylthiourea Reduces Ischemic Brain Edema without Affecting Cerebral Blood Flow
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TLDR
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The results suggest that PBN acts by preventing a gradual compromise of microcirculation and justify a reevaluation of current views on the pathophysiology of focal ischemic damage and suggest that a therapeutic window of many hours exists in stroke.
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