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Int J Mol Sci. 2018 Oct 9;19(10). pii: E3087. doi: 10.3390/ijms19103087.

Inhibition of NADPH Oxidase Activation by Apocynin Rescues Seizure-Induced Reduction of Adult Hippocampal Neurogenesis.

Author information

1
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. sshlee@hallym.ac.kr.
2
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. bychoi@hallym.ac.kr.
3
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. rnlduadkfk136@hallym.ac.kr.
4
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. jd1422@hanmail.net.
5
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. zxnm01220@gmail.com.
6
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. ehdgus2728@naver.com.
7
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. ttiger1993@gmail.com.
8
College of Medicine, Neurology, Hallym University, Chuncheon 24252, Korea. hksong0@hanmail.net.
9
Hallym Institute of Epilepsy Research, Chuncheon 24252, Korea. hksong0@hanmail.net.
10
College of Medicine, Neurology, Hallym University, Chuncheon 24252, Korea. dohchi@naver.com.
11
Hallym Institute of Epilepsy Research, Chuncheon 24252, Korea. dohchi@naver.com.
12
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. swsuh@hallym.ac.kr.
13
Hallym Institute of Epilepsy Research, Chuncheon 24252, Korea. swsuh@hallym.ac.kr.

Abstract

Apocynin, also known as acetovanillone, is a natural organic compound structurally related to vanillin. Apocynin is known to be an inhibitor of NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase activity and is highly effective in suppressing the production of superoxide. The neuroprotective effects of apocynin have been investigated in numerous brain injury settings, such as stroke, traumatic brain injury (TBI), and epilepsy. Our lab has demonstrated that TBI or seizure-induced oxidative injury and neuronal death were reduced by apocynin treatment. Several studies have also demonstrated that neuroblast production is transiently increased in the hippocampus after seizures. Here, we provide evidence confirming the hypothesis that long-term treatment with apocynin may enhance newly generated hippocampal neuronal survival by reduction of superoxide production after seizures. A seizure was induced by pilocarpine [(25 mg/kg intraperitoneal (i.p.)] injection. Apocynin was continuously injected for 4 weeks after seizures (once per day) into the intraperitoneal space. We evaluated neuronal nuclear antigen (NeuN), bromodeoxyuridine (BrdU), and doublecortin (DCX) immunostaining to determine whether treatment with apocynin increased neuronal survival and neurogenesis in the hippocampus after seizures. The present study indicates that long-term treatment of apocynin increased the number of NeuN⁺ and DCX⁺ cells in the hippocampus after seizures. Therefore, this study suggests that apocynin treatment increased neuronal survival and neuroblast production by reduction of hippocampal oxidative injury after seizures.

KEYWORDS:

NADPH-oxidase inhibitor; epilepsy; neurogenesis; neuron death; oxidative stress; pilocarpine

PMID:
30304850
PMCID:
PMC6212849
DOI:
10.3390/ijms19103087
[Indexed for MEDLINE]
Free PMC Article

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