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

Author:

Huang Jun-Jie1ORCID,Feng Yue-Min1ORCID,Zheng Shu-Mei1ORCID,Yu Cheng-Long1ORCID,Zhou Rui-Gang1ORCID,Liu Ming-Jiang12ORCID,Bo Ruo-Nan12ORCID,Yu Jie3ORCID,Li Jin-Gui12ORCID

Affiliation:

1. College of Veterinary Medicine, Yangzhou University, Wenhui East Road 48, Yangzhou 225009, P. R. China

2. Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, P. R. China

3. The Affiliated Suqian First People’s Hospital of Nanjing Medical University, Suzhi Road 120, Suqian 223800, P. R. China

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.

Funder

the National Natural Science Foundation of China

the Postgraduate Research & Practice Innovation Program of Jiangsu Province

Publisher

World Scientific Pub Co Pte Ltd

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