These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Alismol, a Sesquiterpenoid Isolated from Vladimiria souliei, Suppresses Proinflammatory Mediators in Lipopolysaccharide-Stimulated Microglia.
    Author: Shi D, Song X, Guo Y, Xu J, Liu Y, Zhang J, Cui CA, Jin DQ.
    Journal: J Mol Neurosci; 2017 May; 62(1):106-113. PubMed ID: 28474151.
    Abstract:
    Microglia activation plays an important role in the pathogenesis of various neurodegenerative diseases by producing neurotoxic factors, such as proinflammatory cytokines and nitric oxide (NO); therefore, suppression of microglia activation is a potential therapeutic approach against these diseases. Previous study showed that alismol, a sesquiterpenoid isolated from the roots of Vladimiria souliei inhibits interferon-γ-induced NO production in murine macrophage RAW264.7 cells. In the present study, we found that alismol reduced NO and prostaglandin E2 (PGE2) levels and suppressed the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-stimulated primary and cultured microglia. Alismol also inhibited the mRNA and protein expression of proinflammatory cytokines including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Further mechanistic studies revealed that alismol inhibited LPS-induced nuclear factor-κB (NF-κB) activation but not mitogen-activated protein kinase (MAPK) pathway. Finally, we demonstrated the neuroprotective effects of alismol in microglia-neuron coculture systems. Collectively, these results suggest that the inhibition of microglia activation by alismol may provide potential therapeutic strategy for various neuroinflammatory diseases.
    [Abstract] [Full Text] [Related] [New Search]