2015
DOI: 10.1111/cns.12428
|View full text |Cite
|
Sign up to set email alerts
|

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

Abstract: Zn(2+) is involved in neural cell apoptosis and/or death caused by hypoxia/ischemia via mediating excitotoxicity, oxidative stress, and inflammation.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

0
14
0

Year Published

2016
2016
2019
2019

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 25 publications
(14 citation statements)
references
References 67 publications
0
14
0
Order By: Relevance
“…This vesicular zinc may be released by nitrosative stress observed at 8 h after reperfusion and as part of the positive feedback cycle between ROS/RNS generation and increased zinc release [92], causing excitotoxicity [93]. This phenomenon can also result in the loss of long-term memory in rats with CCAO and those chronically pretreated with zinc, in contrast with the improvement in the long-term memory caused by the subacute administration of zinc in rats with CCAO [23].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…This vesicular zinc may be released by nitrosative stress observed at 8 h after reperfusion and as part of the positive feedback cycle between ROS/RNS generation and increased zinc release [92], causing excitotoxicity [93]. This phenomenon can also result in the loss of long-term memory in rats with CCAO and those chronically pretreated with zinc, in contrast with the improvement in the long-term memory caused by the subacute administration of zinc in rats with CCAO [23].…”
Section: Discussionmentioning
confidence: 99%
“…The neuronal injury in the late phase of CCAO might be caused by an excessive accumulation of zinc in presynaptic vesicles and synaptic space of the hippocampus in rats with prophylactic chronic treatment of zinc as previously shown [ 35 ]. This vesicular zinc may be released by nitrosative stress observed at 8 h after reperfusion and as part of the positive feedback cycle between ROS/RNS generation and increased zinc release [ 92 ], causing excitotoxicity [ 93 ]. This phenomenon can also result in the loss of long-term memory in rats with CCAO and those chronically pretreated with zinc, in contrast with the improvement in the long-term memory caused by the subacute administration of zinc in rats with CCAO [ 23 ].…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, based on experiments performed with neuronal tissues, it is believed that rising zinc levels increase hypoxia-mediated cell death occurring during tissue ischemia (120,189). Correspondingly, this effect can be reduced by the Zn 2+ chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethane-1,2-diamine (TPEN) (108,204).…”
Section: Fig 8 Measurement Of Freementioning
confidence: 99%
“…In these conditions, zinc is released in excess by presynaptic neurons and astrocytes, resulting in neuronal death via the activation of microglia, NADPH oxidase and the production of ROS in neurons [ 60 , 61 , 62 ]. Moreover, zinc is also involved in the apoptosis of brain cells induced by hypoxia or ischemia [ 63 ]. This study observed that treatment of cells in vitro and in animals with a zinc chelator, named N,N,N′,N′-Tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), attenuated neurological deficit, reduced the rate of neuronal apoptosis and the cerebral infarct area, increased superoxide dismutase activity and reduced plasma concentrations of malondialdehyde and interleukin-6 (IL-6).…”
Section: Chronic Diseasesmentioning
confidence: 99%