Delavatine A, an unusual isoquinoline alkaloid isolated from I. delavayi, was first studied for antiinflammatory 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-1 beta (1-1 beta) 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-alpha, IL-6, IL-beta. In addition, we examined several pathways related to inflammation. The results revealed that delavatine A significantly decreased LPS-induced the activation of nuclear factor-kappa B (NF-kappa B) by suppressing the p65 subunits, and the phosphorylation of IKBot, while not related to PI3K/Akt or MAPK pathways. (C) 2018 Elsevier Inc. All rights reserved.