Moronic acid improves intestinal inflammation in mice with chronic colitis by inhibiting intestinal macrophage polarization

活性氧 炎症性肠病 脂多糖 巨噬细胞极化 炎症 促炎细胞因子 结肠炎 化学 免疫学 细胞因子 巨噬细胞 生物 体外 医学 生物化学 内科学 疾病
作者
Shuiliang Ruan,Li Zha
出处
期刊:Journal of Biochemical and Molecular Toxicology [Wiley]
卷期号:36 (11) 被引量:3
标识
DOI:10.1002/jbt.23188
摘要

Abstract This study focuses on exploring the role and mechanism of moronic acid (MOA), a small triterpenoid molecule, against inflammatory bowel disease (IBD). Intestinal macrophages were cultured in vitro, and their M1 polarization was induced by lipopolysaccharide (LPS) and interferon gamma (IFN‐γ). After intervention with MOA, the proportion of M1 macrophages was detected, and the levels of inflammatory cytokines (TNF‐α, IL‐6, and IL‐1β) were examined by ELISA. IFA staining was performed to determine the P50 and CD86 expressions, while DCFH‐DA was used to determine the reactive oxygen species (ROS) level, as well as the p‐P50 and NLRP3 protein levels. Additionally, we also used N‐acetylcysteine, a ROS inhibitor, to further explore the association between MOA and ROS‐NF‐κB signaling. In murine experimentation, colitis was induced in mice with DSS. After MOA intervention, we assessed the mucosal barrier damage, tissue ROS, as well as protein and inflammatory cytokine levels. MOA could inhibit the M1 polarization of intestinal macrophages, suppress the expressions of inflammatory cytokines, and reduce the level of ROS‐NF‐κB‐NLRP3 signaling. After inhibiting ROS through NAC treatment, the effect of MOA was evidently weakened. Clearly, MOA exerted its activity via ROS. In the murine model, MOA could lower the CD86 level in the intestinal tissues, inhibit the M1 polarization of macrophages, and reduce the tissue levels of inflammatory cytokines. This study finds that MOA can regulate ROS‐NF‐κB‐NLRP3 signaling by inhibiting ROS, thereby suppressing the M1 polarization of intestinal macrophages, which plays a protective role in IBD.
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