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PLoS One. 2016 Sep 26;11(9):e0163433. doi: 10.1371/journal.pone.0163433. eCollection 2016.

Phlorofucofuroeckol Improves Glutamate-Induced Neurotoxicity through Modulation of Oxidative Stress-Mediated Mitochondrial Dysfunction in PC12 Cells.

Kim JJ1,2,3,4, Kang YJ1, Shin SA2, Bak DH5, Lee JW6, Lee KB7, Yoo YC8, Kim DK9, Lee BH10, Kim DW11,2,3, Lee J11,12, Jo EK11,13, Yuk JM11,12.

Author information

1
Department of Biomedical Science, Jungwon University, Geosan, Chungbuk, South Korea.
2
Anatomy, College of Medicine, Chungnam National University, Daejeon, South Korea.
3
Brain Research Institute, College of Medicine, Chungnam National University, Daejeon, South Korea.
4
LES Corporation Inc., Daejeon, South Korea.
5
Department of Anatomy, College of Medicine, Konyang University, Daejeon, South Korea.
6
Material Science and Engineering, Jungwon University, Geosan, Chungbuk, South Korea.
7
Biochemistry, College of Medicine, Konyang University, Daejeon, South Korea.
8
Microbiology, College of Medicine, Konyang University, Daejeon, South Korea.
9
Pharmacology, College of Medicine, Konyang University, Daejeon, South Korea.
10
Department of Chemical and Biological Engineering, Hanbat National University, Daejeon, South Korea.
11
Department of Medical Science, College of Medicine, Chungnam National University, Daejeon, South Korea.
12
Infection Biology, College of Medicine, Chungnam National University, Daejeon, South Korea.
13
Microbiology, College of Medicine, Chungnam National University, Daejeon, South Korea.

Abstract

Stroke is a complex neurodegenerative disorder with a clinically high prevalence and mortality. Despite many efforts to protect against ischemic stroke, its incidence and related permanent disabilities continue to increase. In this study, we found that pretreatment with phlorofucofuroeckol (PFF), isolated from brown algae species, significantly increased cell viability in glutamate-stimulated PC12 cells. Additionally, glutamate-stimulated cells showed irregular morphology, but PFF pretreatment resulted in improved cell morphology, which resembled that in cells cultured under normal conditions. We further showed that PFF pretreatment effectively inhibited glutamate-induced apoptotic cell death in a caspase-dependent manner. Reactive oxygen species (ROS) induced by oxidative stress are closely associated with ischemia-induced neurological diseases. Exposure of PC12 cells to glutamate induced abundant production of intracellular ROS and mitochondrial dysfunction, which was attenuated by PFF in a dose-dependent manner. In vivo studies revealed that PFF-mediated prevention was achieved predominantly through inhibition of apoptosis and mitochondrial ROS generation. Taken together, these results suggest the possibility of PFF as a neuroprotective agent in ischemic stroke.

Conflict of interest statement

LES Corporation Inc. provided support in the form of salaries for authors JJ Kim, but did not have any additional role in the preparation of material and reagents, the study design, data collection and analysis, decision to publish, or preparation of the manuscript. This commercial affiliation had no role with any other relevant declarations relating to employment, consultancy, patents, products in development, or marketed products, etc. In addition, this relationship does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.

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