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Int J Mol Sci. 2018 Jan 8;19(1). pii: E187. doi: 10.3390/ijms19010187.

Protective Effects of Protocatechuic Acid on Seizure-Induced Neuronal Death.

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. bluesea3616@naver.com.
7
Faculty of Medical Sciences, Western University, London, ON N6A 5C1, Canada. sam8233157@gmail.com.
8
College of Medicine, Neurology, Hallym University, Chuncheon 24252, Korea. minwoo.lee.md@gmail.com.
9
College of Medicine, Neurology, Hallym University, Chuncheon 24252, Korea. hksong0@paran.com.
10
College of Medicine, Neurology, Hallym University, Chuncheon 24252, Korea. dohchi@naver.com.
11
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea. swsuh@hallym.ac.kr.

Abstract

Protocatechuic acid (PCA) is a type of phenolic acid found in green tea and has been shown to have potent antioxidant and anti-inflammatory properties. However, the effect of PCA on pilocarpine seizure-induced neuronal death in the hippocampus has not been evaluated. In the present study, we investigated the potential therapeutic effects of PCA on seizure-induced brain injury. Epileptic seizure was induced by intraperitoneal (i.p.) injection of pilocarpine (25 mg/kg) in adult male rats, and PCA (30 mg/kg) was injected into the intraperitoneal space for three consecutive days after the seizure. Neuronal injury and oxidative stress were evaluated three days after a seizure. To confirm whether PCA increases neuronal survival and reduced oxidative injury in the hippocampus, we performed Fluoro-Jade-B (FJB) staining to detect neuronal death and 4-hydroxynonenal (4HNE) staining to detect oxidative stress after the seizure. In the present study, we found that, compared to the seizure vehicle-treated group, PCA administration reduced neuronal death and oxidative stress in the hippocampus. To verify whether a decrease of neuronal death by PCA treatment was due to reduced glutathione (GSH) concentration, we measured glutathione with N-ethylmaleimide (GS-NEM) levels in hippocampal neurons. A seizure-induced reduction in the hippocampal neuronal GSH concentration was preserved by PCA treatment. We also examined whether microglia activation was affected by the PCA treatment after a seizure, using CD11b staining. Here, we found that seizure-induced microglia activation was significantly reduced by the PCA treatment. Therefore, the present study demonstrates that PCA deserves further investigation as a therapeutic agent for reducing hippocampal neuronal death after epileptic seizures.

KEYWORDS:

epilepsy; microglia; neuron death; oxidative stress; pilocarpine; protocatechuic acid

PMID:
29316696
PMCID:
PMC5796136
DOI:
10.3390/ijms19010187
[Indexed for MEDLINE]
Free PMC Article

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