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

Anti-inflammatory effects of trans-cinnamaldehyde on lipopolysaccharide-stimulated macrophage activation via MAPKs pathway regulation
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DOI:
10.1080/08923973.2018.1424902
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发表时间:
2018-01-01
影响因子:
3.3
通讯作者:
Lee, Jun Sik
Lee, Jun Sik
中科院分区:
医学4区
文献类型:
--
作者:
Kim, Mi Eun;Na, Ju Yong;Lee, Jun Sik

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目的:炎症是先天免疫系统对各种感染的主要反应。巨噬细胞是一种在炎症中起关键作用的免疫细胞。最近的研究报道,各种天然化合物可以调节免疫反应,如炎症。反式肉桂醛(TCA)是肉桂中的一种天然化合物,尤其在肉桂皮中含量丰富。已有研究报道TCA具有抗生物膜、抗微生物和抗癌活性。然而,TCA对巨噬细胞的抗炎作用及其机制尚不清楚。材料和方法:本研究采用小鼠巨噬细胞264.7。主要检测方法有MTT法、Griess法、Western blot法、酶联免疫吸附法(ELISA)和逆转录(RT)-PCR法。结果:本研究考察了TCA对小鼠巨噬细胞RAW 264.7的抗炎作用。TCA以剂量依赖的方式显著降低脂多糖(LPS)诱导的一氧化氮(NO)的产生。此外,TCA处理显著降低lps刺激巨噬细胞诱导型NO合成酶(iNOS) mRNA和蛋白表达,并呈剂量依赖性。TCA处理还降低了lps活化巨噬细胞mRNA表达水平和IL-1 β、IL-6和tnf - α的分泌。TCA通过抑制细胞中ERK、JNK和p38 MPAKs的磷酸化而引起抗炎作用。讨论与结论:TCA通过抑制MAPK5磷酸化和促炎基因表达,对lps刺激的巨噬细胞活化产生抗炎作用。因此,本研究为TCA作为抗炎症候选治疗剂的使用提供了重要信息。
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-1 beta, IL-6 and TNF-alpha 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 MAPK5 phosphorylation, and pro-inflammatory gene expression. Therefore, this study provides important information regarding the use of TCA as a candidate therapeutic agent against inflammation.