Peng Bo, Xue Linyun, Yu Qian, Zhong Tian
Department of Rehabilitation Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, PR China.
Department of Gastroenterology, First Hospital of Putian City, Putian, PR China.
Int J Food Sci Nutr. 2023;74(4):476-486. doi: 10.1080/09637486.2023.2230525. Epub 2023 Jul 16.
In the present study, the mechanism of ellagic acid (EA) in alleviated ulcerative colitis (UC) was investigated. Twenty-four SD rats were randomly distributed into three treatment groups: (1) control group, (2) UC group, and (3) UC + EA group. Samples were collected for analysis after a 15-day trial period. We found that EA mitigated the colitis symptoms in TNBS-treated rats. Besides, EA decreased the expression of cytokines by inhibiting NF-κB signalling. TNBS-induced reduction in tight junction proteins was restored by EA supplementation regulating RhoA/ROCK/MLC signalling. Further, persistent colonic inflammation destroyed the activity of goblet cells by inhibiting the expression of KLF4 and TFF3. EA also enhanced the expression of MUC2, AGR2, ST6GAL1 and B3GNT6. In summary, our findings demonstrated that dietary supplementation with EA ameliorated TNBS-induced colitis by maintaining intestinal barrier function, which proves its potential role as a therapeutic agent in the attenuation of UC.
在本研究中，对鞣花酸（EA）缓解溃疡性结肠炎（UC）的机制进行了研究。将24只SD大鼠随机分为三个治疗组：（1）对照组，（2）UC组，以及（3）UC + EA组。在15天的试验期后收集样本进行分析。我们发现EA减轻了经三硝基苯磺酸（TNBS）处理大鼠的结肠炎症状。此外，EA通过抑制核因子κB（NF-κB）信号传导降低了细胞因子的表达。通过补充EA调节RhoA/ROCK/肌球蛋白轻链（MLC）信号传导，恢复了TNBS诱导的紧密连接蛋白减少。此外，持续性结肠炎症通过抑制Kruppel样因子4（KLF4）和三叶因子3（TFF3）的表达破坏了杯状细胞的活性。EA还增强了黏蛋白2（MUC2）、前梯度蛋白2（AGR2）、α-2,6-唾液酸转移酶1（ST6GAL1）和β-1,3-N-乙酰氨基葡萄糖转移酶6（B3GNT6）的表达。总之，我们的研究结果表明，饮食中补充EA通过维持肠道屏障功能改善了TNBS诱导的结肠炎，这证明了其作为治疗药物在减轻UC方面的潜在作用。
