Abstract |
The neuroprotective effects of superoxide dismutase (SOD) against hypoxia/reperfusion (I/R) injury and of humanin (HN) against toxicity by familial amyotrophic lateral sclerosis (ALS)-related mutant SOD led us to hypothesize that HN might have a role to increase the activity of SOD, which might be involved in the protective effects of HN on neuron against Alzheimer's disease-unrelated neurotoxicities. In the present study, we found that 4 h ischemia and 24 h reperfusion induced a significant increase in lactate dehydrogenase (LDH) release, malondialdehyde (MDA) formation and the number of karyopyknotic nuclei (4',6-diamidino-2-phenylindole dihydrochloride nuclear dyeing) and a decrease in the number of Calcein-AM-positive living cells and cell viability. Pretreatment of the cells with HN led to a significant decrease in LDH release, MDA formation and the number of karyopyknotic nuclei, and an increase in the number of Calcein-AM-positive living cells and cell viability in neurons treated with I/R. We also found a significant decrease in SOD activity in neurons treated with I/R only, while pre-treatment with HN before I/R induced a significant increase in the activity of SOD as compared with the I/R group. Our findings implied that HN protects cortical neurons from I/R injury by the increased SOD activity and that the protective effect of HN on neurons against I/R is concentration-dependent.
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Authors | Shen-Ting Zhao, Xiao-Tian Huang, Ce Zhang, Ya Ke |
Journal | Neurochemical research
(Neurochem Res)
Vol. 37
Issue 1
Pg. 153-60
(Jan 2012)
ISSN: 1573-6903 [Electronic] United States |
PMID | 21935731
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Intracellular Signaling Peptides and Proteins
- humanin
- Malondialdehyde
- L-Lactate Dehydrogenase
- Superoxide Dismutase
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Topics |
- Cerebral Cortex
(cytology, enzymology, metabolism)
- Humans
- Intracellular Signaling Peptides and Proteins
(physiology)
- L-Lactate Dehydrogenase
(metabolism)
- Malondialdehyde
(metabolism)
- Neurons
(cytology, enzymology, metabolism)
- Reperfusion Injury
(pathology)
- Superoxide Dismutase
(metabolism)
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