Delavatine A, an unusual isoquinoline alkaloid exerts anti-inflammation on LPS-induced proinflammatory cytokines production by suppressing NF-κB activation in BV-2 microglia

Delavatine A, an unusual isoquinoline alkaloid exerts anti-inflammation on LPS-induced... Delavatine A, an unusual isoquinoline alkaloid isolated from I. delavayi, was first studied for anti-inflammatory effect using lipopolysaccharide (LPS)-induced BV-2 microglia. In the present study, we found that delavatine A substantially suppressed the LPS-induced pro-inflammatory mediators, nitric oxide (NO), and tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), interleukin-1β (IL-1β) in BV-2 microglial cells. These effects resulted from the inhibition of their regulatory genes inducible NO synthase (iNOS), cycloxygenase-2 (COX-2) and TNF-a, IL-6, IL-1β. In addition, we examined several pathways related to inflammation. The results revealed that delavatine A significantly decreased LPS-induced the activation of nuclear factor-κB (NF-κB) by suppressing the p65 subunits, and the phosphorylation of IκBα, while not related to PI3K/Akt or MAPK pathways. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochemical and Biophysical Research Communications Elsevier

Delavatine A, an unusual isoquinoline alkaloid exerts anti-inflammation on LPS-induced proinflammatory cytokines production by suppressing NF-κB activation in BV-2 microglia

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier Inc.
ISSN
0006-291x
D.O.I.
10.1016/j.bbrc.2018.05.144
Publisher site
See Article on Publisher Site

Abstract

Delavatine A, an unusual isoquinoline alkaloid isolated from I. delavayi, was first studied for anti-inflammatory effect using lipopolysaccharide (LPS)-induced BV-2 microglia. In the present study, we found that delavatine A substantially suppressed the LPS-induced pro-inflammatory mediators, nitric oxide (NO), and tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), interleukin-1β (IL-1β) in BV-2 microglial cells. These effects resulted from the inhibition of their regulatory genes inducible NO synthase (iNOS), cycloxygenase-2 (COX-2) and TNF-a, IL-6, IL-1β. In addition, we examined several pathways related to inflammation. The results revealed that delavatine A significantly decreased LPS-induced the activation of nuclear factor-κB (NF-κB) by suppressing the p65 subunits, and the phosphorylation of IκBα, while not related to PI3K/Akt or MAPK pathways.

Journal

Biochemical and Biophysical Research CommunicationsElsevier

Published: Jul 12, 2018

References

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