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Chelating Intracellularly Accumulated Zinc Decreased Ischemic Brain Injury Through Reducing Neuronal Apoptotic Death
Author(s) -
Yongmei Zhao,
Rong Pan,
Sen Li,
Yumin Luo,
Feng Yan,
Jie Yin,
Zhifeng Qi,
Ying Yan,
Xunming Ji,
Ke Jian Liu
Publication year - 2014
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.113.004296
Subject(s) - medicine , ischemia , neuroprotection , pharmacology , intracellular , stroke (engine) , zinc , apoptosis , brain ischemia , reperfusion injury , anesthesia , endocrinology , biochemistry , biology , chemistry , mechanical engineering , organic chemistry , engineering
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.

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