Eugenol Possesses Colitis Protective Effects: Impacts on the TLR4/MyD88/NF-[Formula: see text]B Pathway, Intestinal Epithelial Barrier, and Macrophage Polarization.

The American journal of Chinese medicine Pub Date : 2024-01-01 Epub Date: 2024-03-14 DOI:10.1142/S0192415X24500216
Jun-Jie Huang, Yue-Min Feng, Shu-Mei Zheng, Cheng-Long Yu, Rui-Gang Zhou, Ming-Jiang Liu, Ruo-Nan Bo, Jie Yu, Jin-Gui Li
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Abstract

Eugenol (EU) has been shown to ameliorate experimental colitis due to its anti-oxidant and anti-inflammatory bioactivities. In this study, DSS-induced acute colitis was established and applied to clarify the regulation efficacy of EU on intestinal barrier impairment and macrophage polarization imbalance along with the inflammatory response. Besides, the adjusting effect of EU on macrophages was further investigated in vitro. The results confirmed that EU intervention alleviated DSS-induced colitis through methods such as restraining weight loss and colonic shortening and decreasing DAI scores. Microscopic observation manifested that EU maintained the intestinal barrier integrity in line with the mucus barrier and tight junction protection. Furthermore, EU intervention significantly suppressed the activation of TLR4/MyD88/NF-[Formula: see text]B signaling pathways and pro-inflammatory cytokines gene expressions, while enhancing the expressions of anti-inflammatory cytokines. Simultaneously, WB and FCM analyses of the CD86 and CD206 showed that EU could regulate the DSS-induced macrophage polarization imbalance. Overall, our data further elucidated the mechanism of EU's defensive effect on experimental colitis, which is relevant to the protective efficacy of intestinal barriers, inhibition of oxidative stress and excessive inflammatory response, and reprogramming of macrophage polarization. Hence, this study may facilitate a better understanding of the protective action of the EU against UC.

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丁香酚具有保护结肠炎的作用:对 TLR4/MyD88/NF-[式中:见正文]B 通路、肠上皮屏障和巨噬细胞极化的影响
丁香酚(EU)具有抗氧化和抗炎的生物活性,可改善实验性结肠炎。本研究建立并应用了 DSS 诱导的急性结肠炎,以明确丁香酚对肠道屏障损伤和巨噬细胞极化失衡以及炎症反应的调节作用。此外,还在体外进一步研究了欧盟对巨噬细胞的调节作用。结果证实,通过抑制体重下降、结肠缩短和降低DAI评分等方法,欧盟干预可减轻DSS诱导的结肠炎。显微镜观察表明,欧盟维持了肠道屏障的完整性,具有粘液屏障和紧密连接保护作用。此外,欧盟干预明显抑制了 TLR4/MyD88/NF-[配 方:见正文]B信号通路的激活和促炎细胞因子基因的表达,同时提高了抗炎细胞因子的表达。同时,CD86和CD206的WB和FCM分析表明,EU能调节DSS诱导的巨噬细胞极化失衡。总之,我们的数据进一步阐明了欧盟对实验性结肠炎的防御作用机制,该机制与保护肠道屏障、抑制氧化应激和过度炎症反应以及重编程巨噬细胞极化有关。因此,这项研究可能有助于更好地理解欧盟对 UC 的保护作用。
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