Protective mechanisms of CA074-me (other than cathepsin-B inhibition) against programmed necrosis induced by global cerebral ischemia/reperfusion injury in rats
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- 作者：Yang Xua ; 1 ; Jingye Wangb ; 1 ; Xinghui Songc ; Ruili Weia ; Fangping Hea ; Guoping Penga ; Benyan Luoa ; luobenyan@zju.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：4-VO ; four-vessel occlusion ; CA1 ; cornu ammonis 1 ; IF ; immunofluorescence ; CCAs ; common carotid arteries ; H&E ; hematoxylin/eosin ; Hsp70 ; heat shock protein 70 ; I/R ; ischemia and reperfusion ; MCAO ; middle cerebral artery occlusion ; LAMP-1/2 ; lysosome-associated membrane protein-1/2 ; LMP ; lysosomal membrane permeabilization ; NAD ; nicotinamide adenine dinucleotide ; OGD ; oxygen-glucose deprivation ; OD ; optical density ; PVDF ; polyvinylidene fluoride ; RIP3 ; receptor-interacting protein 3 ; ROS ; reactiv
- 刊名：Brain Research Bulletin
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：120
- 期：Complete
- 页码：97-105
- 全文大小：2491 K
文摘
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Delayed fulminant leakage of cathepsin-B by lysosomal rupture is a critical harmful factor in delayed neuronal programmed necrosis induced by 20-min global I/R injury.
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In addition to being an inhibitor of cathepsin-B, CA074-me may have an indirect neuroprotective effect on maintaining lysosomal membrane integrity.
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CA074-me prevent delayed neuronal programmed necrosis by enhancing the expression of Hsp70 and inhibiting the reduction of NAD+ level.
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CA074-me treatment inhibits the overexpression and nuclear translocation of RIP3.