Investigating anti-neuroinflammatory mechanism of orientin in lipopolysaccharide-induced BV2 microglia cells

Chronic neuroinflammation in central nervous system (CNS) can lead to neurodegenerative diseases (ND). This was due to the over-activated microglia, which releases excessive pro-inflammatory mediators. The molecular mechanisms of orientin as anti-neuroinflammatory are yet to be fully elucidated. In...

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Published in:Asia-Pacific journal of molecular biology and biotechnology Vol. 27; no. 2; p. 78
Main Authors: Gana, Pei Hong, Laerea, Erna, Linga, Anna Pick Kiong, Voonb, Kenny Gah Leong, Koha, Rhun Yian, Wonga, Ying Pei
Format: Journal Article
Language:English
Published: Kuala Lumpur Malaysian Society for Molecular Biology and Biotechnology 01-01-2019
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Summary:Chronic neuroinflammation in central nervous system (CNS) can lead to neurodegenerative diseases (ND). This was due to the over-activated microglia, which releases excessive pro-inflammatory mediators. The molecular mechanisms of orientin as anti-neuroinflammatory are yet to be fully elucidated. In order to investigate the effect of orientin on LPS-stimulated BV2 microglial cells, the cells were pretreated with orientin at maximum non-toxic dose (MNTD) (15 µM) or half MNTD (½ MNTD) (7.5 µM) for 3 hours, followed by incubation with 0.1 µg/mL of LPS for 24 hours. The LPS-stimulated cells were then subjected to three series of studies, including the determination of ROS level using 2',7'- dichlorofluorescindiacetate (DCFH-DA) methods and the determination of mRNA of nuclear factor (NF)- кB, Signal transducer and activator of transcription 1 (STAT1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)and heme oxygenase-1 (HO-1) via real-time PCR (qPCR). The findings from this study demonstrated the probable mechanism of orientin in treating neuroinflammation via the downregulation of ROS level, STAT1, NF-кB, iNOS and COX-2 whilst upregulating HO-1. Validation of molecular mechanism of orientin suggested that it could be a potential therapeutic agent in treating ND.
ISSN:0128-7451