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

OBJECTIVE

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.

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.

CONCLUSIONS

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.