Chen Shuang, Zhang Chun-Lei, Shen Hai-Qing, Zhou Xiao-Fei, Li Jing-He, Yu Jia-Lin, An Qiang, Fu Ben-Dong, Yi Peng-Fei
College of Veterinary Medicine, Jilin University, 5333 Xi'an Road, Changchun, Jilin 130062, China.
Food Funct. 2021 Mar 1;12(4):1688-1694. doi: 10.1039/d0fo00950d.
To investigate the protective effects and mechanisms of sesamin (SES) on dextran sulfate sodium (DSS)-induced experimental colitis in mice.
SES (50, 100, and 200 mg kg-1) were orally administered to C57BL/6 male mice after DSS instillation. The anti-inflammatory effect of SES on colonic damage was assessed by clinical, macroscopic, microscopic, and inflammatory signaling pathways.
It could be found that bodyweight and colon length of mice treated with DSS was significantly decreased while that were increased by SES treatment. SES treatment reduced the DAI values and improved the histopathology of the colon in the DSS-treated mice. SES also reduced TNF-α, IL-1β and IL-6 production caused by DSS. We also measured the expression of the phosphorylation of p65, IκB, p38, ERK and JNK protein and found that SES can alleviate colon damage via the NF-κB and MAPK signaling pathways. The findings of this study suggested that SES had anti-inflammatory effects on intestinal inflammation and can be used as a new therapeutic candidate for inflammatory bowel disease.
研究芝麻素（SES）对葡聚糖硫酸钠（DSS）诱导的小鼠实验性结肠炎的保护作用及机制。
DSS灌胃后，对C57BL/6雄性小鼠口服给予SES（50、100和200 mg kg-1）。通过临床、宏观、微观和炎症信号通路评估SES对结肠损伤的抗炎作用。
发现DSS处理的小鼠体重和结肠长度显著降低，而SES处理使其增加。SES处理降低了DSS处理小鼠的疾病活动指数（DAI）值，改善了结肠组织病理学。SES还降低了DSS引起的肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的产生。我们还检测了p65、IκB、p38、细胞外调节蛋白激酶（ERK）和应激活化蛋白激酶（JNK）蛋白磷酸化的表达，发现SES可通过核因子-κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号通路减轻结肠损伤。本研究结果表明，SES对肠道炎症具有抗炎作用，可作为炎症性肠病的一种新的治疗候选药物。
