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Biochim Biophys Acta. 2014 Jul;1840(7):2321-30. doi: 10.1016/j.bbagen.2014.03.003. Epub 2014 Mar 12.

Neuroprotective effect of PEP-1-peroxiredoxin2 on CA1 regions in the hippocampus against ischemic insult.

Author information

1
Department of Biomedical Sciences, Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea.
2
Department of Anatomy and Cell Biology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul 151-742, Republic of Korea.
3
Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Kangnung-Wonju National University, Gangneung 210-702, Republic of Korea.
4
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, Republic of Korea.
5
Department of Anatomy and Cell Biology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul 151-742, Republic of Korea. Electronic address: vetmed2@snu.ac.kr.
6
Department of Biomedical Sciences, Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea. Electronic address: sychoi@hallym.ac.kr.

Abstract

BACKGROUND:

Oxidative stress is a leading cause of various diseases, including ischemia and inflammation. Peroxiredoxin2 (PRX2) is one of six mammalian isoenzymes (PRX1-6) that can reduce hydrogen peroxide (H2O2) and organic hydroperoxides to water and alcohols.

METHODS:

We produced PEP-1-PRX2 transduction domain (PTD)-fused protein and investigated the effect of PEP-1-PRX2 on oxidative stress-induced neuronal cell death by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Western blot, immunofluorescence microscopy, and immunohistochemical analysis.

RESULTS:

Our data showed that PEP-1-PRX2, which can effectively transduce into various types of cells and brain tissues, could be implicated in suppressing generation of reactive oxygen species, preventing depolarization of the mitochondrial membrane, and inhibiting the apoptosis pathway in H2O2-stimulated HT22, murine hippocampal neuronal cells, likely resulting in protection of HT22 cells against H2O2-induced toxicity. In addition, we found that in a transient forebrain ischemia model, PEP-1-PRX2 inhibited the activation of astrocytes and microglia in the CA1 region of the hippocampus and lipid peroxidation and also prevented neuronal cell death against ischemic damage.

CONCLUSIONS:

These findings suggest that the transduced PEP-1-PRX2 has neuroprotective functions against oxidative stress-induced cell death in vitro and in vivo.

GENERAL SIGNIFICANCE:

PEP-1-PRX2 could be a potential therapeutic agent for oxidative stress-induced brain diseases such as ischemia.

KEYWORDS:

Apoptosis pathway; Ischemic insult; Oxidative stress; Peroxiredoxin2; Protein transduction domain

PMID:
24631653
DOI:
10.1016/j.bbagen.2014.03.003
[Indexed for MEDLINE]
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