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https://hdl.handle.net/20.500.14094/0100485308
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2024-06-08
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0100485308 (fulltext)
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0100485308
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open access
出版タイプ
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タイトル
Luteolin Protects Against 6-Hydoroxydopamine-Induced Cell Death via an Upregulation of HRD1 and SEL1L
著者
Nishiguchi, Hiroki ; Omura, Tomohiro ; Sato, Ayaka ; Kitahiro, Yumi ; Yamamoto, Kazuhiro ; Kunimasa, Junichi ; Yano, Ikuko
著者名
Nishiguchi, Hiroki
著者ID
A2517
研究者ID
1000000439035
ORCID
0000-0001-5520-253X
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=2d29530d752c12b2520e17560c007669
著者名
Omura, Tomohiro
大村, 友博
オオムラ, トモヒロ
所属機関名
医学部附属病院
著者名
Sato, Ayaka
著者ID
A3251
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=85d804befdb62b4d520e17560c007669
著者名
Kitahiro, Yumi
北廣, 優実
キタヒロ, ユミ
所属機関名
医学部附属病院
著者ID
A2417
研究者ID
1000030610349
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=be897871e34ee593520e17560c007669
著者名
Yamamoto, Kazuhiro
山本, 和宏
ヤマモト, カズヒロ
所属機関名
医学部附属病院
著者名
Kunimasa, Junichi
著者ID
A0421
研究者ID
1000050273446
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=c67473c1ec5daab2520e17560c007669
著者名
Yano, Ikuko
矢野, 育子
ヤノ, イクコ
所属機関名
医学部附属病院
収録物名
Neurochemical Research
巻(号)
49(1)
ページ
117-128
出版者
Springer Nature
刊行日
2024-01
公開日
2023-11-29
抄録
Parkinson's Disease (PD) is caused by many factors and endoplasmic reticulum (ER) stress is considered as one of the responsible factors for it. ER stress induces the activation of the ubiquitin-proteasome system to degrade unfolded proteins and suppress cell death. The ubiquitin ligase 3-hydroxy-3-methylglutaryl-coenzyme A reductase degradation 1 (HRD1) and its stabilizing molecule, the suppressor/enhancer lin-12-like (SEL1L), can suppress the ER stress via the ubiquitin-proteasome system, and that HRD1 can also suppress cell death in familial and nonfamilial PD models. These findings indicate that HRD1 and SEL1L might be key proteins for the treatment of PD. Our study aimed to identify the compounds with the effects of upregulating the HRD1 expression and suppressing neuronal cell death in a 6-hydroxydopamine (6-OHDA)-induced cellular PD model. Our screening by the Drug Gene Budger, a drug repositioning tool, identified luteolin as a candidate compound for the desired modulation of the HRD1 expression. Subsequently, we confirmed that low concentrations of luteolin did not show cytotoxicity in SH-SY5Y cells, and used these low concentrations in the subsequent experiments. Next, we demonsrated that luteolin increased HRD1 and SEL1L mRNA levels and protein expressions. Furthermore, luteolin inhibited 6-OHDA-induced cell death and suppressed ER stress response caused by exposure to 6-OHDA. Finally, luteolin did not reppress 6-OHDA-induced cell death when expression of HRD1 or SEL1L was suppressed by RNA interference. These findings suggest that luteolin might be a novel therapeutic agent for PD due to its ability to suppress ER stress through the activation of HRD1 and SEL1L.
キーワード
luteolin
Parkinson’s disease
endoplasmic reticulum stress
HRD1
SEL1L
カテゴリ
医学部附属病院
学術雑誌論文
権利
© The Author(s) 2023
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.
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資源タイプ
journal article
言語
English (英語)
ISSN
0364-3190
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eISSN
1573-6903
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関連情報
DOI
https://doi.org/10.1007/s11064-023-04019-2
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