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論文
- タイトル
- タイトル（英）
- Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1
- 参照URL
- https://researchmap.jp/351K/published_papers/39823133
- 著者
- 著者（英）
- Yasuaki Tatsumi,Ayako Kato,Naoko Niimi,Hideji Yako,Tatsuhito Himeno,Masaki Kondo,Shin Tsunekawa,Yoshiro Kato,Hideki Kamiya,Jiro Nakamura,Koji Higai,Kazunori Sango,Koichi Kato
- 担当区分
- 概要
- 概要（英）
- Autophagy is the process by which intracellular components are degraded by lysosomes. It is also activated by oxidative stress; hence, autophagy is thought to be closely related to oxidative stress, one of the major causes of diabetic neuropathy. We previously reported that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) induced antioxidant enzymes and protected Schwann cells from oxidative stress. However, the relationship between autophagy and oxidative stress-induced cell death in diabetic neuropathy has not been elucidated. Treatment with tert-butyl hydroperoxide (tBHP) decreased the cell survival rate, as measured by an MTT assay in immortalized Fischer rat Schwann cells 1 (IFRS1). A DHA pretreatment significantly prevented tBHP-induced cytotoxicity. tBHP increased autophagy, which was revealed by the ratio of the initiation markers, AMP-activated protein kinase, and UNC51-like kinase phosphorylation. Conversely, the DHA pretreatment suppressed excessive tBHP-induced autophagy signaling. Autophagosomes induced by tBHP in IFRS1 cells were decreased to control levels by the DHA pretreatment whereas autolysosomes were only partially decreased. These results suggest that DHA attenuated excessive autophagy induced by oxidative stress in Schwann cells and may be useful to prevent or reduce cell death in vitro. However, its potentiality to treat diabetic neuropathy must be validated in in vivo studies.
- 出版者・発行元
- 出版者・発行元（英）
- MDPI AG
- 誌名
- 誌名（英）
- International Journal of Molecular Sciences
- 巻
- 23
- 号
- 8
- 開始ページ
- 4405
- 終了ページ
- 4405
- 出版年月
- 2022年4月15日
- 査読の有無
- 査読有り
- 招待の有無
- 掲載種別
- 研究論文（学術雑誌）
- ISSN
- DOI URL
- https://doi.org/10.3390/ijms23084405
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