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Article

Lipoxin A4 Receptor Stimulation Attenuates Neuroinflammation in a Mouse Model of Intracerebral Hemorrhage

1
Laboratory of Pharmacology and Neurobiology, Collage of Pharmaceutical Sciences, Ritsumeikan University, 1-1-1 Noji-Higashi, Kusatsu 525-8577, Japan
2
Department of Pharmacology II, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women’s University, 11-68 Koshien Kyuban-cho, Nishinomiya 663-8179, Japan
3
Department of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan
*
Author to whom correspondence should be addressed.
Academic Editors: Lindsay T. Michalovicz and Kimberly A. Kelly
Brain Sci. 2022, 12(2), 162; https://doi.org/10.3390/brainsci12020162
Received: 4 January 2022 / Revised: 22 January 2022 / Accepted: 24 January 2022 / Published: 26 January 2022
(This article belongs to the Special Issue Neuroinflammation in Neurological Diseases)
Intracerebral hemorrhage (ICH) is caused by the rupture of blood vessels in the brain. The excessive activation of glial cells and the infiltration of numerous inflammatory cells are observed during bleeding. Thrombin is a key molecule that triggers neuroinflammation in the ICH brain. In this study, we focused on lipoxin A4 (LXA4), an arachidonic acid metabolite that has been reported to suppress inflammation and cell migration. LXA4 and BML-111, an agonist of the LXA4 receptor/formyl peptide receptor 2 (ALX/FPR2), suppressed microglial activation; LXA4 strongly inhibited the migration of neutrophil-like cells in vitro. ALX/FPR2 was expressed on neutrophils in the ICH mouse brain and the daily administration of BML-111 attenuated the motor coordination dysfunction and suppressed the production of proinflammatory cytokines in the ICH mouse brain. On the other hand, BML-111 did not show a significant reduction in the number of microglia and neutrophils. These results suggest that systemic administration of ALX/FPR2 agonists may suppress the neuroinflammatory response of microglia and neutrophils without a change in cell numbers. Additionally, their combination with molecules that reduce cell numbers, such as modulators of leukotriene B4 signaling, may be required in future studies. View Full-Text
Keywords: intracerebral hemorrhage; neuroinflammation; lipoxin A4; neutrophil; microglia intracerebral hemorrhage; neuroinflammation; lipoxin A4; neutrophil; microglia
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MDPI and ACS Style

Futokoro, R.; Hijioka, M.; Arata, M.; Kitamura, Y. Lipoxin A4 Receptor Stimulation Attenuates Neuroinflammation in a Mouse Model of Intracerebral Hemorrhage. Brain Sci. 2022, 12, 162. https://doi.org/10.3390/brainsci12020162

AMA Style

Futokoro R, Hijioka M, Arata M, Kitamura Y. Lipoxin A4 Receptor Stimulation Attenuates Neuroinflammation in a Mouse Model of Intracerebral Hemorrhage. Brain Sciences. 2022; 12(2):162. https://doi.org/10.3390/brainsci12020162

Chicago/Turabian Style

Futokoro, Risa, Masanori Hijioka, Moe Arata, and Yoshihisa Kitamura. 2022. "Lipoxin A4 Receptor Stimulation Attenuates Neuroinflammation in a Mouse Model of Intracerebral Hemorrhage" Brain Sciences 12, no. 2: 162. https://doi.org/10.3390/brainsci12020162

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