Abstract
Here, we investigated the role of LXRα in capsaicin mediated anti-inflammatory effects. Results revealed that capsaicin inhibits LPS-induced IL-1β, IL-6 and TNF-α production in a time- and dose-dependent manner. Moreover, capsaicin increases LXRα expression through PPARγ pathway. Inhibition of LXRα activation by siRNA diminished the inhibitory action of capsaicin on LPS-induced IL-1β, IL-6 and TNF-α production. Additionally, LXRα siRNA abrogated the inhibitory action of capsaicin on p65 NF-κB protein expression. Thus, we propose that the anti-inflammatory effects of capsaicin are LXRα dependent, and LXRα may potentially link the capsaicin mediated PPARγ activation and NF-κB inhibition in LPS-induced inflammatory response.
Keywords:
Capsaicin; Inflammation; LXRα; NF-κB; PPARγ.
Copyright © 2015 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
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Capsaicin / pharmacology*
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Cells, Cultured
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Cytokines / biosynthesis*
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Dose-Response Relationship, Drug
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Humans
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Interleukin-1beta / biosynthesis
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Interleukin-6 / biosynthesis
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Lipopolysaccharides / antagonists & inhibitors*
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Liver X Receptors
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Orphan Nuclear Receptors / biosynthesis*
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Orphan Nuclear Receptors / drug effects
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Orphan Nuclear Receptors / genetics
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PPAR gamma / drug effects
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RNA, Small Interfering / pharmacology
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Transcription Factor RelA / biosynthesis
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Transcription Factor RelA / drug effects
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Tumor Necrosis Factor-alpha / biosynthesis
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Up-Regulation / drug effects
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cytokines
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IL1B protein, human
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IL6 protein, human
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Interleukin-1beta
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Interleukin-6
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Lipopolysaccharides
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Liver X Receptors
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NR1H3 protein, human
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Orphan Nuclear Receptors
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PPAR gamma
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RNA, Small Interfering
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Transcription Factor RelA
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Tumor Necrosis Factor-alpha
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Capsaicin