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Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death

Authors :
Song Hee Lee
Sang Won Suh
Jeong Hyun Jeong
Sang Hwon Lee
A Ra Kho
Dae Ki Hong
Bo Young Choi
Source :
International Journal of Molecular Sciences, International Journal of Molecular Sciences; Volume 18; Issue 12; Pages: 2510, International Journal of Molecular Sciences, Vol 18, Iss 12, p 2510 (2017)
Publication Year :
2017

Abstract

Protocatechuic acid (PCA) was first purified from green tea and has shown numerous biological activities, including anti-apoptotic, anti-inflammatory, and anti-atherosclerotic effects. The effect of PCA on traumatic brain injury (TBI)-induced neuronal death has not previously been evaluated. TBI is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. TBI causes neuronal death in the hippocampus and cerebral cortex. The present study aimed to evaluate the therapeutic potential of PCA on TBI-induced neuronal death. Here, TBI was induced by a controlled cortical impact model using rats. PCA (30 mg/kg) was injected into the intraperitoneal (ip) space immediately after TBI. Neuronal death was evaluated with Fluoro Jade-B (FJB) staining at 24 h after TBI. Oxidative injury was detected by 4-hydroxy-2-nonenal (4HNE), glutathione (GSH) concentration was analyzed by glutathione adduct with N-ethylmaleimide (GS-NEM) staining at 24 h after TBI, and microglial activation in the hippocampus was detected by CD11b immunohistochemistry at one week after TBI. We found that the proportion of degenerating neurons, oxidative injury, GSH depletion, and microglia activation in the hippocampus and cortex were all reduced by PCA treatment following TBI. Therefore, our study suggests that PCA may have therapeutic potential in preventing TBI-induced neuronal death.

Details

ISSN :
14220067
Volume :
18
Issue :
12
Database :
OpenAIRE
Journal :
International journal of molecular sciences
Accession number :
edsair.doi.dedup.....d36ee55ae5f5450d1055a5046152927c