Anti-inflammatory effects of trans-cinnamaldehyde on lipopolysaccharide-stimulated macrophage activation via MAPKs pathway regulation.

OBJECTIVES: Inflammation is a primary response of the innate immune system against various infections. Macrophages are a type of immune cell that have a critical role in the inflammation. Recent studies reported that various natural compounds could regulate immune responses such as inflammation. Trans-cinnamaldehyde (TCA) is a natural compound from cinnamon, especially abundant in cinnamon bark. Previous studies reported that TCA has anti-biofilm, anti-microbial, and anti-cancer activities. However, the anti-inflammatory effects and the mechanism of TCA on macrophages are still unknown.

MATERIALS AND METHODS: Raw 264.7 murine macrophage cells were used in this study. Major assays were MTT, Griess assay, Western blot, enzyme-linked immunosorbent assay (ELISA) and reverse transcription (RT)-PCR analysis.

RESULTS: In this study, we investigated the anti-inflammatory effects of TCA on the RAW 264.7 murine macrophage cell line. TCA significantly decreased lipopolysaccharide (LPS)-induced nitric oxide (NO) production in a dose-dependent manner. Moreover, TCA treatment significantly reduced mRNA expression and protein expression of inducible NO synthase (iNOS) in LPS-stimulated macrophages in a dose-dependent manner. TCA treatment also diminished the mRNA expression level and secretion of IL-1β, IL-6 and TNF-α in LPS-activated macrophages. TCA elicited the anti-inflammatory effects by inhibiting ERK, JNK and p38 MPAKs phosphorylation in the cells.

DISCUSSION AND CONCLUSION: TCA elicits the anti-inflammatory effects on LPS-stimulated macrophage activation via suppression of MAPKs phosphorylation, and pro-inflammatory gene expression. Therefore, this study provides important information regarding the use of TCA as a candidate therapeutic agent against inflammation.