Ex vivo imaging and analysis of ROS generation correlated with microglial activation in rat model with acute neuroinflammation induced by intrastriatal injection of LPS.


Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
20 12 2021
Historique:
received: 01 09 2021
accepted: 02 11 2021
pubmed: 16 11 2021
medline: 4 1 2022
entrez: 15 11 2021
Statut: ppublish

Résumé

Neuroinflammation and oxidative stress are hallmarks of neurodegenerative diseases. Microglia, the major important regulators of neuroinflammation, are activated in response to excessive generation of reactive oxygen species (ROS) from damaged cells and resulting in elevated and sustained damages. However, the relationship between microglia and ROS-regulatory system in the early stages of neuroinflammation prior to the appearance of neuronal damages have not been elucidated in detail. In this study, we analyzed the time-dependent changes in ROS generation during acute neuroinflammation in rats that were given an intrastriatal injection of lipopolysaccharide (LPS). We evaluated the effects of minocycline, an anti-inflammatory antibiotic, and N,N'-dimethylthiourea (DMTU), a radical scavenger, to understand the correlation between activated microglia and ROS generation. Ex vivo fluorescence imaging using dihydroethidium (DHE) clearly demonstrated an increased ROS level in the infused side of striatum in the rats treated with LPS. The level of ROS was changed in time-dependent manner, and the highest level of ROS was observed on day 3 after the infusion of LPS. Immunohistochemical studies revealed that time-dependent changes in ROS generation were well correlated to the presence of activated microglia. The inhibition of microglial activation by minocycline remarkably reduced ROS levels in the LPS-injected striatum, which indicated that the increased ROS generation caused by LPS was induced by activated microglia. DMTU decreased ROS generation and resulted in remarkable inhibitory effect on microglial activation. This study demonstrated that ROS generation during acute neuroinflammation induced by LPS was considerably associated with microglial activation, in an intact rat brain. The results provides a basis for understanding the interaction of ROS-regulatory system and activated microglia during neuroinflammation underlying neurodegenerative diseases.

Identifiants

pubmed: 34781201
pii: S0006-291X(21)01511-4
doi: 10.1016/j.bbrc.2021.11.008
pii:
doi:

Substances chimiques

Fluorescent Dyes 0
Free Radical Scavengers 0
Lipopolysaccharides 0
Reactive Oxygen Species 0
dihydroethidium 104821-25-2
1,3-dimethylthiourea 8P30PMD17W
Ethidium EN464416SI
Minocycline FYY3R43WGO
Thiourea GYV9AM2QAG

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

101-106

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no competing of interest.

Auteurs

Miho Shukuri (M)

Laboratory of Physical Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo, 194-8543, Japan. Electronic address: shukuri@ac.shoyaku.ac.jp.

Miyu Uchino (M)

Laboratory of Physical Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo, 194-8543, Japan.

Takafumi Sakamaki (T)

Laboratory of Physical Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo, 194-8543, Japan.

Satoru Onoe (S)

Laboratory of Physical Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo, 194-8543, Japan. Electronic address: onoe@ac.shoyaku.ac.jp.

Rie Hosoi (R)

Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita, Osaka, 565-0871, Japan. Electronic address: hosoi@sahs.med.osaka-u.ac.jp.

Kenichiro Todoroki (K)

Department of Analytical and Bio-Analytical Chemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka, 422-8526, Japan. Electronic address: todoroki@u-shizuoka-ken.ac.jp.

Yasushi Arano (Y)

Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8675, Japan. Electronic address: arano@chiba-u.jp.

Toshihiro Sakai (T)

Hanwa Intelligent Medical Center, Hanwa Daini Senboku Hospital, 3176 Fukaikitamachi, Naka-ku, Sakai, Osaka, 599-8271, Japan. Electronic address: sakai.toshihiro@kinshukai.or.jp.

Hiromichi Akizawa (H)

Laboratory of Physical Chemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo, 194-8543, Japan. Electronic address: aki@ac.shoyaku.ac.jp.

Osamu Inoue (O)

Hanwa Intelligent Medical Center, Hanwa Daini Senboku Hospital, 3176 Fukaikitamachi, Naka-ku, Sakai, Osaka, 599-8271, Japan. Electronic address: inoue.osamu@kinshukai.or.jp.

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Classifications MeSH