医学
TLR4型
炎症
经络
溃疡性结肠炎
结肠炎
信号转导
药理学
免疫学
炎症性肠病
节点2
促炎细胞因子
免疫系统
癌症研究
先天免疫系统
内科学
疾病
生物
木犀草素
类黄酮
细胞生物学
生物化学
抗氧化剂
作者
Lihong Hu,Jingyang Liu,Yin Jia
摘要
Ulcerative colitis (UC) is a chronic disease characterized by mucosal and submucosal inflammation, which has a low cure rate and is prone to relapse, due to the immune imbalance of the body. Inhibition of inflammation-related pathways can delay the progression of UC. Toll-like receptor 4 (TLR4) pathway is considered to be one of the important signaling pathways involved in colon inflammation. Eriodictyol (EDT) is a natural flavonoid widely distributed in foodborne plants. EDT plays an important role in the regulation of inflammation and related signaling pathways. However, whether EDT plays a role in UC remains unknown. Herein, we established a TNBS induced animal model of enteritis in Wistar rats. Our data confirmed the establishment of TNBS induced animal model of enteritis and the administration Eriodictyol in Wistar rats. EDT treatment alleviated TNBS-induced intestinal tissue injury in rats. We further found that EDT reduced MPO expression and regulated the cytokine parameters in TNBS-induced intestinal tissues of rats. The levels of TNF-α, IL-1β, IL-6, IL-10, IL-2, and IL-12 were also affected by the treatment of EDT. EDT also affected SOD, CAT, GSH-Px, and MDA level in rats with colitis. Moreover, EDT regulated TNBS-induced TLR4/NF-κB pathway activation, therefore inhibiting the progression of UC. Our results suggest that EDT could be a potential therapeutic agent for UC.
科研通智能强力驱动
Strongly Powered by AbleSci AI