Eugenol Possesses Colitis Protective Effects: Impacts on the TLR4/MyD88/NF-κB Pathway, Intestinal Epithelial Barrier, and Macrophage Polarization

TLR4型 结肠炎 丁香酚 NF-κB 巨噬细胞极化 巨噬细胞 化学 信号转导 医学 免疫学 生物化学 体外 有机化学
作者
J. Huang,Yue-Min Feng,Shu-Mei Zheng,Cheng-Long Yu,Rui-Gang Zhou,Mingjiang Liu,Ruonan Bo,Jie Yu,Jingui Li
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:52 (02): 493-512 被引量:7
标识
DOI:10.1142/s0192415x24500216
摘要

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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