Methyl p-Hydroxycinnamate Suppresses Lipopolysaccharide-Induced Inflammatory Responses through Akt Phosphorylation in RAW264.7 Cells

Vo, Van Anh; Lee, Jae-Won; Shin, Seung-Yeon; Kwon, Jae-Hyun; Lee, Hee Jae; Kim, Sung-Soo; Kwon, Yong-Soo; Chun, Wanjoo

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자료유형: 학술저널

저자정보: Vo, Van Anh (Department of Pharmacology, College of Medicine, Kangwon National University) Lee, Jae-Won (Department of Pharmacology, College of Medicine, Kangwon National University) Shin, Seung-Yeon (Department of Pharmacology, College of Medicine, Kangwon National University) Kwon, Jae-Hyun (Department of Pharmacology, College of Medicine, Kangwon National University) Lee, Hee Jae (Department of Pharmacology, College of Medicine, Kangwon National University) Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) Kwon, Yong-Soo (College of Pharmacy, Kangwon National University) Chun, Wanjoo (Department of Pharmacology, College of Medicine, Kangwon National University)

저널정보: 한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제22권 제1호

발행연도: 2014.1

수록면: 10 - 16 (7page)

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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 $PGE_2$ and the protein expression of iNOS and COX-2. Methyl p-hydroxycinnamate also suppressed LPS-induced overproduction of pro-inflammatory cytokines such as IL-$1{\beta}$ and TNF-${\alpha}$. In addition, methyl p-hydroxycinnamate significantly suppressed LPS-induced degradation of $I{\kappa}B$, which retains NF-${\kappa}B$ in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-${\kappa}B$ 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.

#Methyl p-hydroxycinnamate #RAW 264 #7 cells #Lipopolysaccharide #iNOS #COX-2 #NF- ${kappa}B$

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