Methyl p-Hydroxycinnamate Suppresses Lipopolysaccharide-Induced Inflammatory Responses through Akt Phosphorylation in RAW264.7 Cells
Biomolecules & Therapeutics
; : 10-16, 2014.
Article
in En
| WPRIM
| ID: wpr-138521
Responsible library:
WPRO
ABSTRACT
Derivatives of caffeic acid have been reported to possess diverse pharmacological properties such as anti-inflammatory, anti-tumor, and neuroprotective effects. However, the biological activity of methyl p-hydroxycinnamate, an ester derivative of caffeic acid, has not been clearly demonstrated. This study aimed to elucidate the anti-inflammatory mechanism of methyl p-hydroxycinnamate in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Methyl p-hydroxycinnamate significantly inhibited LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein expression of iNOS and COX-2. Methyl p-hydroxycinnamate also suppressed LPS-induced overproduction of pro-inflammatory cytokines such as IL-1beta and TNF-alpha. In addition, methyl p-hydroxycinnamate significantly suppressed LPS-induced degradation of IkappaB, which retains NF-kappaB in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-kappaB in the nucleus. Methyl p-hydroxycinnamate exhibited significantly increased Akt phosphorylation in a concentration-dependent manner. Furthermore, inhibition of Akt signaling pathway with wortmaninn abolished methyl p-hydroxycinnamate-induced Akt phosphorylation. Taken together, the present study clearly demonstrates that methyl p-hydroxycinnamate exhibits anti-inflammatory activity through the activation of Akt signaling pathway in LPS-stimulated RAW264.7 macrophage cells.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Phosphorylation
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Dinoprostone
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Cytokines
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NF-kappa B
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Tumor Necrosis Factor-alpha
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Neuroprotective Agents
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Cytoplasm
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Macrophages
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Nitric Oxide
Language:
En
Journal:
Biomolecules & Therapeutics
Year:
2014
Type:
Article