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Cited 12 time in webofscience Cited 11 time in scopus
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The small molecule CA140 inhibits the neuroinflammatory response in wild-type mice and a mouse model of AD

Authors
Lee, Ju-YoungNam, Jin HanNam, YoungpyoNam, Hye YeonYoon, GwanghoKo, EunhwaKim, Sang-BumBautista, Mahealani R.Capule, Christina C.Koyanagi, TakaokiLeriche, GeoffrayChoi, Hwan GeunYang, JerryKim, JeongyeonHoe, Hyang-Sook
Issue Date
Oct-2018
Publisher
BMC
Keywords
Alzheimer' s disease; Neuroinflammation; D1R; ERK; STAT3; LPS; CA140
Citation
JOURNAL OF NEUROINFLAMMATION, v.15
Journal Title
JOURNAL OF NEUROINFLAMMATION
Volume
15
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/723
DOI
10.1186/s12974-018-1321-3
ISSN
1742-2094
Abstract
Background: Neuroinflammation is associated with neurodegenerative diseases, including Alzheimer's disease (AD). Thus, modulating the neuroinflammatory response represents a potential therapeutic strategy for treating neurodegenerative diseases. Several recent studies have shown that dopamine (DA) and its receptors are expressed in immune cells and are involved in the neuroinflammatory response. Thus, we recently developed and synthesized a non-self-polymerizing analog of DA (CA140) and examined the effect of CA140 on neuroinflammation. Methods: To determine the effects of CA140 on the neuroinflammatory response, BV2 microglial cells were pretreated with lipopolysaccharide (LPS, 1 mu g/mL), followed by treatment with CA140 (10 mu M) and analysis by reverse transcription-polymerase chain reaction (RT-PCR). To examine whether CA140 alters the neuroinflammatory response in vivo, wild-type mice were injected with both LPS (10 mg/kg, intraperitoneally (i.p.)) and CA140 (30 mg/kg, i.p.), and immunohistochemistry was performed. In addition, familial AD (5xFAD) mice were injected with CA140 or vehicle daily for 2weeks and examined for microglial and astrocyte activation. Results: Pre- or post-treatment with CA140 differentially regulated proinflammatory responses in LPS-stimulated microglia and astrocytes. Interestingly, CA140 regulated D1R levels to alter LPS-induced proinflammatory responses. CA140 significantly downregulated LPS-induced phosphorylation of ERK and STAT3 in BV2 microglia cells. In addition, CA140-injected wild-type mice exhibited significantly decreased LPS-induced microglial and astrocyte activation. Moreover, CA140-injected 5xFAD mice exhibited significantly reduced microglial and astrocyte activation. Conclusions: CA140 may be beneficial for preventing and treating neuroinflammatory-related diseases, including AD.
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연구본부 > 정서·인지 질환 연구그룹 > 1. Journal Articles

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연구본부 (정서·인지질환 연구그룹)
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