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ORIGINAL RESEARCH article

Front. Pharmacol.
Sec. Inflammation Pharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1416350
This article is part of the Research Topic Targeting Neuroinflammation for Novel Therapeutics in Neurodegenerative Diseases View all 3 articles

Melatonin Modulates Neuroinflammatory Response and Microglial Activation in Mice Exposed to Dim Blue Light at Night

Provisionally accepted
Chao Song Chao Song 1Zhaotaize Suo Zhaotaize Suo 2Zixu Wang Zixu Wang 1Jing Cao Jing Cao 1Yulan Dong Yulan Dong 1Yaoxing Chen Yaoxing Chen 1*
  • 1 China Agricultural University, Beijing, China
  • 2 High School Affiliated to Renmin University of China, Beijing, China

The final, formatted version of the article will be published soon.

    Objectives: Dim light at night contributes to neurodegenerative diseases by causing neuroinflammation. In the central nervous system, the activation of microglia is a significant contributor to neuroinflammation. Therefore, there is an urgent need to find an intervention to treat the neuroinflammatory response caused by dim light at night. Melatonin is a rhythmic hormone whose synthesis is suppressed during the day. In this study, we attempt to explore whether and how melatonin improves hippocampal neuroinflammation in mice exposed to dim blue light at night.In vivo, a total of 36 male C57BL6/J mice that exposed to no light at night, dim blue light at night, and dim blue light at night with melatonin treatment. In vitro, the corticosterone-induced BV2 cells with or without melatonin treatment were used.Results: Both in vivo and in vitro experiments showed melatonin treatment significantly reduced dim blue light -induced hippocampal microglial activation and the expression of inflammatory factors IL-1β and TNF-α. This improved effect of melatonin is related to its receptor MT2 rather than MT1. The MT2 blockers significantly increased mRNA levels of M1-type activation marker CD86 and inflammatory cytokines IL-1β and TNF-α in melatonin-treated BV2 cells. Binding of melatonin to its receptor MT2 downregulated the expression of inflammatory proteins P-P65 and NLRP3, consequently inhibited the CD80 expression and M1-type activation in microglia. Furthermore, consistent with the decrease in microglial activation and inflammatory response after melatonin treatment, we also observed a reduction in hippocampal neuron loss and damage to the HT22 cells.Our findings suggested that melatonin may regulate microglial polarization through MT2/NF-kB-NLRP3 pathway and improves dim blue light -induced hippocampal neuroinflammation in mice.

    Keywords: d-BL, Melatonin, MT2, Microglia, Neuroinflammation

    Received: 12 Apr 2024; Accepted: 02 May 2024.

    Copyright: © 2024 Song, Suo, Wang, Cao, Dong and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Yaoxing Chen, China Agricultural University, Beijing, China

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