School of Chinese Medicine, Hong Kong Baptist University , Kowloon Tong, Hong Kong, People's Republic of China.
J Nat Prod. 2013 Nov 22;76(11):2120-5. doi: 10.1021/np4006772. Epub 2013 Nov 7.
The therapeutic effect of corilagin (1) was evaluated in an acute colitis model induced by dextran sulfate sodium (DSS) in mice, and the mechanism of action was investigated in this study. Animals were challenged with 2% DSS drinking water for 5 consecutive days and then intraperitoneally treated with 1 (7.5, 15, and 30 mg/kg) daily for 7 days. It was found that 1 significantly decreased the disease activity index, inhibited the shortening of colon length, reduced colon tissue damage, and suppressed myeloperoxidase activity. Moreover, 1 greatly suppressed the secretion of TNF-α, IL-6, and IL-1β, inhibited the degradation of IκB α, and down-regulated expression of cleaved caspase-3 and cleaved caspase-9 in colon tissues of DSS-treated mice. These findings demonstrated that 1 exerts a protective effect on DSS-induced colitis, and its underlying mechanisms are associated with inhibition of the NF-κB pathway that mitigates colon inflammatory responses and apoptosis of intestinal epithelial cells.
鞣花酸(1)在小鼠葡聚糖硫酸钠(DSS)诱导的急性结肠炎模型中的治疗效果进行了评估,并在本研究中研究了其作用机制。动物用 2% DSS 饮用水连续 5 天处理,然后每天腹膜内给予 1(7.5、15 和 30 mg/kg)治疗 7 天。结果发现,1 可显著降低疾病活动指数,抑制结肠长度缩短,减轻结肠组织损伤,并抑制髓过氧化物酶活性。此外,1 还可显著抑制 TNF-α、IL-6 和 IL-1β的分泌,抑制 IκBα的降解,并下调 DSS 处理的小鼠结肠组织中 cleaved caspase-3 和 cleaved caspase-9 的表达。这些发现表明 1 对 DSS 诱导的结肠炎具有保护作用,其作用机制与抑制 NF-κB 通路有关,该通路减轻了结肠炎症反应和肠上皮细胞的凋亡。