Biomol Ther.
2014 Jan;22(1):10-16.
Methyl p-Hydroxycinnamate Suppresses Lipopolysaccharide-Induced Inflammatory Responses through Akt Phosphorylation in RAW264.7 Cells
- Affiliations
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- 1Department of Pharmacology, College of Medicine, Kangwon National University, Chuncheon 200-701, Republic of Korea. wchun@kangwon.ac.kr
- 2College of Pharmacy, Kangwon National University, Chuncheon 200-701, Republic of Korea.
- 3Department of Radiology, Dongguk University Ilsan Hospital, Ilsan 410-773, Republic of Korea.
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.
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