- 著者
- 
             
             Miki Nagata
             
             Mayumi Tsuji
             
             Tatsunori Oguchi
             
             Yutaro Momma
             
             Tetsuhito Nohara
             
             Hideaki Ohashi
             
             Naohito Ito
             
             Ken Yamamoto
             
             Yuko Udaka
             
             Akiko Sasaki
             
             Yuji Kiuchi
             
             Satoshi Numazawa
             
          
- 出版者
- The Pharmaceutical Society of Japan
- 雑誌
- BPB Reports (ISSN:2434432X)
- 巻号頁・発行日
- vol.4, no.6, pp.206-213, 2021 (Released:2021-12-27)
- 参考文献数
- 41
- 被引用文献数
- 
             
             
             2
             
             
          
        
        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.