Panaxytriol Inhibits Lipopolysaccharide-Induced Microglia Activation in Brain Inflammation in Vivo

Brain inflammation is a pathological characteristic of neurodegenerative diseases. In this condition, excessively activated microglia elevate proinflammatory mediator levels. We previously reported that panaxytriol inhibited lipopolysaccharide (LPS)-induced microglia activation in vitro. However, th...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2021/07/01, Vol.44(7), pp.1024-1028
Main Authors: Hiramatsu, Genki, Matsuda, Kosuke, Uta, Daisuke, Mihara, Kenichi, Kume, Toshiaki
Format: Article
Language:English
Subjects:
Animals
Astrocytes
Astrocytes - drug effects
brain inflammation
Encephalitis - drug therapy
Enediynes - pharmacology
Enediynes - therapeutic use
Fatty Alcohols - pharmacology
Fatty Alcohols - therapeutic use
Hippocampus - drug effects
Inflammation
lipopolysaccharide
Lipopolysaccharides
Lipopolysaccharides - pharmacology
Locomotion - drug effects
Mice
Mice, Inbred C57BL
Microglia
Microglia - drug effects
microglia activation
Motor activity
Neurodegenerative diseases
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
panaxytriol
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Summary:Brain inflammation is a pathological characteristic of neurodegenerative diseases. In this condition, excessively activated microglia elevate proinflammatory mediator levels. We previously reported that panaxytriol inhibited lipopolysaccharide (LPS)-induced microglia activation in vitro. However, the effects of panaxytriol on microglia activation in vivo require confirmation. In the present study, we found that panaxytriol suppressed both microglia and astrocyte activation by injected LPS intracerebrally to mice with LPS-induced brain inflammation. Panaxytriol was more effective on microglia than astrocytes. Moreover, panaxytriol tended to reduce LPS-induced spontaneous motor activity dysfunction. These results suggested that panaxytriol could improve brain health by suppressing microglia activation in neurodegenerative diseases.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b21-00288