Protective effects of Nrf2-ARE activator on dopaminergic neuronal loss in Parkinson disease model mice: Possible involvement of heme oxygenase-1.


Journal

Neuroscience letters
ISSN: 1872-7972
Titre abrégé: Neurosci Lett
Pays: Ireland
ID NLM: 7600130

Informations de publication

Date de publication:
25 09 2020
Historique:
received: 04 05 2020
revised: 09 07 2020
accepted: 20 07 2020
pubmed: 28 7 2020
medline: 1 5 2021
entrez: 27 7 2020
Statut: ppublish

Résumé

Parkinson disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra, and oxidative stress is thought to contribute to this pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway, which induces the production of antioxidant enzymes, is thereby a potential target for therapeutics to reduce neurodegeneration in PD. Previously, we identified TPNA10168 from a chemical library as an activator of the Nrf2-ARE pathway, and the present study examined the effects of TPNA10168 on an in vivo PD model. Subcutaneous administration of TPNA10168 was associated with inhibited dopaminergic neuronal loss and behavioral impairment in 6-hydroxydopamine-induced PD model mice. Heme oxygenase-1 (HO-1) is an antioxidant enzyme expressed downstream of the Nrf2-ARE signaling pathway, and we observed that HO-1 protein levels were upregulated by TPNA10168 in the mouse brain. These results suggest that TPNA10168 inhibits dopaminergic neuronal death in PD model mice, and that upregulation of HO-1 might participate in this effect.

Identifiants

pubmed: 32712353
pii: S0304-3940(20)30538-3
doi: 10.1016/j.neulet.2020.135268
pii:
doi:

Substances chimiques

NF-E2-Related Factor 2 0
Nfe2l2 protein, mouse 0
Oxidopamine 8HW4YBZ748
Heme Oxygenase-1 EC 1.14.14.18

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

135268

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Yuri Inose (Y)

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8501, Japan.

Yasuhiko Izumi (Y)

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8501, Japan; Laboratory of Pharmacology, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Higashinada-ku, Kobe, 658-8558, Japan.

Yuki Takada-Takatori (Y)

Faculty of Pharmaceutical Sciences, Doshisha Women's College, Kodo, Kyotanabe-shi, Kyoto, 610-0395, Japan.

Akinori Akaike (A)

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8501, Japan; Wakayama Medical University, Japan.

Yutaka Koyama (Y)

Laboratory of Pharmacology, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Higashinada-ku, Kobe, 658-8558, Japan.

Shuji Kaneko (S)

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8501, Japan.

Toshiaki Kume (T)

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Shimoadachi-cho, Sakyo-ku, Kyoto, 606-8501, Japan; Department of Applied Pharmacology, Graduate School of Medical and Pharmaceutical Science, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. Electronic address: tkume@pha.u-toyama.ac.jp.

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