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Anti-inflammatory mechanism of α-viniferin regulates lipopolysaccharide-induced release of proinflammatory mediators in BV2 microglial cells

 Matharage Gayani Dilshara  ;  Kyoung-Tae Lee  ;  Hee Ju Kim  ;  Hak-Ju Lee  ;  Yung Hyun Choi  ;  Chang-Min Lee  ;  Lark Kyun Kim  ;  Gi-Young Kim 
 CELLULAR IMMUNOLOGY, Vol.290(1) : 21-29, 2014 
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Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology* ; Benzofurans/pharmacology* ; Cell Line ; Clematis ; Cyclooxygenase 2/biosynthesis* ; Dinoprostone/biosynthesis ; Heme Oxygenase-1/biosynthesis ; Heme Oxygenase-1/immunology ; Inflammation Mediators ; Lipopolysaccharides ; Membrane Proteins/biosynthesis ; Membrane Proteins/immunology ; Mice ; Microglia/immunology* ; NF-E2-Related Factor 2/biosynthesis ; NF-E2-Related Factor 2/genetics ; NF-kappa B/antagonists & inhibitors* ; NF-kappa B/genetics ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase Type II/biosynthesis* ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/immunology ; Phosphorylation ; Plant Extracts ; Plant Roots ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/immunology ; Pyrrolidines/pharmacology ; RNA Interference ; RNA, Small Interfering ; Thiocarbamates/pharmacology
α-Viniferin is an oligostilbene of trimeric resveratrol and has anticancer activity; however, the molecular mechanism underlying the anti-inflammatory effects of α-viniferin has not been completely elucidated thus far. Therefore, we determined the mechanism by which α-viniferin regulates lipopolysaccharide (LPS)-induced expression of proinflammatory mediators in BV2 microglial cells. Treatment with α-viniferin isolated from Clematis mandshurica decreased LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2). α-Viniferin also downregulated the LPS-induced expression of proinflammatory genes such as iNOS and COX-2 by suppressing the activity of nuclear factor kappa B (NF-κB) via dephosphorylation of Akt/PI3K. Treatment with a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), indirectly showed that NF-κB is a crucial transcription factor for expression of these genes in the early stage of inflammation. Additionally, our results indicated that α-viniferin suppresses NO and PGE2 production in the late stage of inflammation through induction of heme oxygenase-1 (HO-1) regulated by nuclear factor erythroid 2-related factor (Nrf2). Taken together, our data indicate that α-viniferin suppresses the expression of proinflammatory genes iNOS and COX-2 in the early stage of inflammation by inhibiting the Akt/PI3K-dependent NF-κB activation and inhibits the production of proinflammatory mediators NO and PGE2 in the late stage by stimulating Nrf2-mediated HO-1 signaling pathway in LPS-stimulated BV2 microglial cells. These results suggest that α-viniferin may be a potential candidate to regulate LPS-induced inflammation.
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1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kim, Lark Kyun(김락균) ORCID logo https://orcid.org/0000-0001-5983-4470
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