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The MAO Inhibitor Tranylcypromine Alters LPS- and A beta-Mediated Neuroinflammatory Responses in Wild-type Mice and a Mouse Model of AD

Title
The MAO Inhibitor Tranylcypromine Alters LPS- and A beta-Mediated Neuroinflammatory Responses in Wild-type Mice and a Mouse Model of AD
Authors
Park, HyunHeeHan, Kyung-MinJeon, HyongjunLee, Ji-SooLee, HyunjuJeon, Seong GakPark, Jin-HeeKim, Yu GyungLin, YuxiLee, Young-HoJeong, Yun HaHoe, Hyang-Sook
DGIST Authors
Park, HyunHee; Han, Kyung-Min; Jeon, Hyongjun; Lee, Ji-Soo; Lee, Hyunju; Jeon, Seong Gak; Park, Jin-Hee; Kim, Yu Gyung; Lin, Yuxi; Lee, Young-Ho; Jeong, Yun Ha; Hoe, Hyang-Sook
Issue Date
2020-09
Citation
Cells, 9(9), 1982
Type
Article
Article Type
Article
Author Keywords
microgliaamyloid betaLPSneuroinflammationMAO inhibitor
Keywords
MONOAMINE-OXIDASE INHIBITORSNITRIC-OXIDEDISEASECELLSACETYLCHOLINESTERASEANTIDEPRESSANTSANTIOXIDANTDERIVATIVESACTIVATIONPHENELZINE
ISSN
2073-4409
Abstract
Monoamine oxidase (MAO) has been implicated in neuroinflammation, and therapies targeting MAO are of interest for neurodegenerative diseases. The small-molecule drug tranylcypromine, an inhibitor of MAO, is currently used as an antidepressant and in the treatment of cancer. However, whether tranylcypromine can regulate LPS- and/or Aβ-induced neuroinflammation in the brain has not been well-studied. In the present study, we found that tranylcypromine selectively altered LPS-induced proinflammatory cytokine levels in BV2 microglial cells but not primary astrocytes. In addition, tranylcypromine modulated LPS-mediated TLR4/ERK/STAT3 signaling to alter neuroinflammatory responses in BV2 microglial cells. Importantly, tranylcypromine significantly reduced microglial activation as well as proinflammatory cytokine levels in LPS-injected wild-type mice. Moreover, injection of tranylcypromine in 5xFAD mice (a mouse model of AD) significantly decreased microglial activation but had smaller effects on astrocyte activation. Taken together, our results suggest that tranylcypromine can suppress LPS- and Aβ-induced neuroinflammatory responses in vitro and in vivo.
URI
http://hdl.handle.net/20.500.11750/12798
DOI
10.3390/cells9091982
Publisher
NLM (Medline)
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