BPB Reports

Paper Details

BPB Reports
Vol. 4 No. 6 p.206-213 2021
Regular Article
Protective Effects of the Alga Fucoidan Against Amyloid-β-Induced Neurotoxicity in SH-SY5Y Cells
  • Mayumi Tsuji (Pharmacological Research Center, Showa University / tsujim@med.showa-u.ac.jp)
Miki Nagata 1) 2) , Mayumi Tsuji 2) , Tatsunori Oguchi 2) 3) , Yutaro Momma 2) 3) , Tetsuhito Nohara 2) 3) , Hideaki Ohashi 2) 3) , Naohito Ito 2) 3) , Ken Yamamoto 2) 3) , Yuko Udaka 2) 3) , Akiko Sasaki 2) 3) , Yuji Kiuchi 2) 3) , Satoshi Numazawa 1) 2)
1) Division of Toxicology, Department of Pharmacology, Toxicology and Therapeutics, Showa University School of Pharmacy , 2) Pharmacological Research Center, Showa University , 3) Department of Pharmacology, Division of Medical Pharmacology, School of Medicine, Showa University
Received: November 16, 2021;   Accepted: December 13, 2021;   Released: December 27, 2021
Keywords: Alzheimer's disease, amyloid β-protein, fucoidan, oxidative stress, neurotoxicity

Dementia is expected to affect an increasing number of patients with global aging populations. About 70% of all dementia is related to Alzheimer's disease (AD). Overaccumulation of amyloid-β protein (Aβ) in the brain forms senile plaques, one of the main features of neurodegeneration in AD. However, there are few drugs available to specifically inhibit senile plaque formation. Fucoidan, a sulfated polysaccharide derived from brown algae, has various bioactivities, such as anti-tumoral and anti-obesity effects. This study aimed to clarify the mechanism underlying the protective effect of fucoidan against Aβ-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Cell viability and Aβ-induced cytotoxicity were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, calcein AM, and ethidium homodimer-1. Aβ-induced oxidative stress was evaluated through reactive oxygen species (ROS), cell membrane phospholipid peroxidation, mitochondrial ROS, and Mn-SOD, a mitochondrial radical scavenger. In addition, mitochondrial membrane permeability transition, and ATP concentration were evaluated. Fucoidan significantly improved Aβ-reduced cell viability. With respect to oxidative stress, Aβ exposure increased ROS, lipid peroxidation, and mitochondrial ROS, while fucoidan significantly suppressed these changes. Fucoidan also suppressed the decline in mitochondrial permeability transition and ATP caused by Aβ. Therefore, through its numerous antioxidant activities, fucoidan might have a neuroprotective role in preventing Aβ-induced neurotoxicity.