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Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1

1
Laboratory of Medicine, Aichi Gakuin University School of Pharmacy, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan
2
Department of Medical Biochemistry, Faculty of Pharmaceutical Sciences, Toho University, Miyama 2-2-1, Funabashi 274-8510, Japan
3
Diabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya, Tokyo 156-8506, Japan
4
Division of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: David Della-Morte
Int. J. Mol. Sci. 2022, 23(8), 4405; https://doi.org/10.3390/ijms23084405
Received: 18 October 2021 / Revised: 5 April 2022 / Accepted: 14 April 2022 / Published: 15 April 2022
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. View Full-Text
Keywords: DHA; oxidative stress; autophagy; AMPK; Schwann cells DHA; oxidative stress; autophagy; AMPK; Schwann cells
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MDPI and ACS Style

Tatsumi, Y.; Kato, A.; Niimi, N.; Yako, H.; Himeno, T.; Kondo, M.; Tsunekawa, S.; Kato, Y.; Kamiya, H.; Nakamura, J.; Higai, K.; Sango, K.; Kato, K. Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1. Int. J. Mol. Sci. 2022, 23, 4405. https://doi.org/10.3390/ijms23084405

AMA Style

Tatsumi Y, Kato A, Niimi N, Yako H, Himeno T, Kondo M, Tsunekawa S, Kato Y, Kamiya H, Nakamura J, Higai K, Sango K, Kato K. Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1. International Journal of Molecular Sciences. 2022; 23(8):4405. https://doi.org/10.3390/ijms23084405

Chicago/Turabian Style

Tatsumi, Yasuaki, Ayako Kato, Naoko Niimi, Hideji Yako, Tatsuhito Himeno, Masaki Kondo, Shin Tsunekawa, Yoshiro Kato, Hideki Kamiya, Jiro Nakamura, Koji Higai, Kazunori Sango, and Koichi Kato. 2022. "Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1" International Journal of Molecular Sciences 23, no. 8: 4405. https://doi.org/10.3390/ijms23084405

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