Literature DB >> 24643405

Chelating intracellularly accumulated zinc decreased ischemic brain injury through reducing neuronal apoptotic death.

Yongmei Zhao1, Rong Pan, Sen Li, Yumin Luo, Feng Yan, Jie Yin, Zhifeng Qi, Ying Yan, Xunming Ji, Ke Jian Liu.   

Abstract

BACKGROUND AND
PURPOSE: Zinc has been reported to possess both neurotoxic and neuroprotective capabilities. The effects of elevated intracellular zinc accumulation following transient focal cerebral ischemia remain to be fully elucidated. Here, we investigated whether removing zinc with the membrane-permeable zinc chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), would decrease the intracellular levels of zinc in the ischemic tissue, leading to reduced brain damage and improved neurological outcomes.
METHODS: Rats were pretreated with TPEN or vehicle before or after a 90-minute middle cerebral artery occlusion. Cerebral infarct volume, neurological functions, neuronal apoptosis, poly(ADP-ribose) polymerase activity, and cytosolic labile zinc were assessed after ischemia and reperfusion.
RESULTS: Cerebral ischemia caused a dramatic cytosolic labile zinc accumulation in the ischemic tissue, which was decreased markedly by TPEN (15 mg/kg) pretreatment. Chelating zinc lead to reduced infarct volume compared with vehicle-treated middle cerebral artery occlusion rats, accompanied by much improved neurological assessment and motor function, which were sustained for 14 days after reperfusion. We also determined that reducing zinc accumulation rescued neurons from ischemia-induced apoptotic death by reducing poly(ADP-ribose) polymerase-1 activation.
CONCLUSIONS: Ischemia-induced high accumulation of intracellular zinc significantly contributed to ischemic brain damage through promotion of neuronal apoptotic death. Removing zinc may be an effective and novel approach to reduce ischemic brain injury.

Entities:  

Keywords:  brain ischemia; infarction, middle cerebral artery; poly(ADP-ribose) polymerases; zinc

Mesh:

Substances:

Year:  2014        PMID: 24643405     DOI: 10.1161/STROKEAHA.113.004296

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  20 in total

1.  Synergistic Interaction Between Zinc and Reactive Oxygen Species Amplifies Ischemic Brain Injury in Rats.

Authors:  Yongmei Zhao; Feng Yan; Jie Yin; Rong Pan; Wenjuan Shi; Zhifeng Qi; Yalan Fang; Yuyou Huang; Sen Li; Yumin Luo; Xunming Ji; Ke Jian Liu
Journal:  Stroke       Date:  2018-09       Impact factor: 7.914

2.  Zinc cytotoxicity induces mitochondrial morphology changes in hela cell line.

Authors:  Katherine A Knies; Yang V Li
Journal:  Int J Physiol Pathophysiol Pharmacol       Date:  2021-04-15

3.  Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.

Authors:  Wen Dong; Zhifeng Qi; Jia Liang; Wenjuan Shi; Yongmei Zhao; Yumin Luo; Xunming Ji; Ke Jian Liu
Journal:  Exp Neurol       Date:  2015-04-17       Impact factor: 5.330

4.  TPEN, a Specific Zn2+ Chelator, Inhibits Sodium Dithionite and Glucose Deprivation (SDGD)-Induced Neuronal Death by Modulating Apoptosis, Glutamate Signaling, and Voltage-Gated K+ and Na+ Channels.

Authors:  Feng Zhang; Xue-Ling Ma; Yu-Xiang Wang; Cong-Cong He; Kun Tian; Hong-Gang Wang; Di An; Bin Heng; Lai-Hua Xie; Yan-Qiang Liu
Journal:  Cell Mol Neurobiol       Date:  2016-03-16       Impact factor: 5.046

5.  Normobaric Hyperoxia Extends Neuro- and Vaso-Protection of N-Acetylcysteine in Transient Focal Ischemia.

Authors:  Yushan Liu; Wen-Cao Liu; Yanyun Sun; Xianzhi Shen; Xiaona Wang; Hui Shu; Rong Pan; Chun-Feng Liu; Wenlan Liu; Ke Jian Liu; Xinchun Jin
Journal:  Mol Neurobiol       Date:  2016-05-13       Impact factor: 5.590

6.  The Zinc Ion Chelating Agent TPEN Attenuates Neuronal Death/apoptosis Caused by Hypoxia/ischemia Via Mediating the Pathophysiological Cascade Including Excitotoxicity, Oxidative Stress, and Inflammation.

Authors:  Wei-Ming Wang; Zhao Liu; Ai-Jun Liu; Yu-Xiang Wang; Hong-Gang Wang; Di An; Bin Heng; Lai-Hua Xie; Jun-Li Duan; Yan-Qiang Liu
Journal:  CNS Neurosci Ther       Date:  2015-07-20       Impact factor: 5.243

7.  Excessive Zinc Ion Caused PC12 Cell Death Correlating with Inhibition of NOS and Increase of RAGE in Cells.

Authors:  Sai-Ya Zhang; Jing-Jing Liang; Yan-Qiang Liu
Journal:  Cell Biochem Biophys       Date:  2022-09-06       Impact factor: 2.989

Review 8.  The interaction of zinc and the blood-brain barrier under physiological and ischemic conditions.

Authors:  Zhifeng Qi; Ke Jian Liu
Journal:  Toxicol Appl Pharmacol       Date:  2018-12-27       Impact factor: 4.219

9.  TPEN exerts selective anti-leukemic efficacy in ex vivo drug-resistant childhood acute leukemia.

Authors:  Miguel Mendivil-Perez; Carlos Velez-Pardo; Gloria E David-Yepes; Javier E Fox; Marlene Jimenez-Del-Rio
Journal:  Biometals       Date:  2020-10-24       Impact factor: 2.949

10.  Endogenous zinc protoporphyrin formation critically contributes to hemorrhagic stroke-induced brain damage.

Authors:  Rong Pan; Song Yu; Haikun Zhang; Graham S Timmins; John Weaver; Yirong Yang; Xixi Zhou; Ke Jian Liu
Journal:  J Cereb Blood Flow Metab       Date:  2021-06-29       Impact factor: 6.960

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