Department of Oriental Pharmacy, College of Pharmacy, and Wonkwang Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Biol Pharm Bull. 2012;35(5):666-71. doi: 10.1248/bpb.35.666.
Chelidonic acid (CA), a constituent of Chelidonium majus L., has many pharmacological effects, including mild analgesic and antimicrobial effects. However, the effects of CA on intestinal inflammation and the molecular mechanisms responsible are poorly understood. The aim of this study was to investigate the protective effects of CA against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). Mice treated with DSS displayed obvious clinic signs, such as, body weight loss and a shortening of colon length, but the administration of CA attenuated both of these signs. Additionally, CA was found to regulate levels of interleukin-6 and tumor necrosis factor-α in serum. In colonic tissues, prostaglandin E(2) (PGE(2)) production levels and cyclooxygenase-2 (COX-2) and hypoxia induced factor-1α (HIF-1α) expression levels were increased by DSS, but CA attenuated increases in COX-2 and HIF-1α levels. These results provide novel insights into the pharmacological actions of CA and its potential use for the treatment of intestinal inflammation.
没食子酸（CA）是白屈菜Chelidonium majus L. 的一种成分，具有许多药理作用，包括轻度的镇痛和抗菌作用。然而，CA 对肠道炎症的作用及其相关的分子机制尚不清楚。本研究旨在探讨 CA 对葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）的保护作用。用 DSS 处理的小鼠表现出明显的临床症状，如体重减轻和结肠长度缩短，但 CA 的给药减轻了这两种症状。此外，CA 被发现可调节血清中白细胞介素-6 和肿瘤坏死因子-α的水平。在结肠组织中，DSS 增加前列腺素 E（2）（PGE（2））的产生水平以及环氧化酶-2（COX-2）和缺氧诱导因子-1α（HIF-1α）的表达水平，但 CA 可减弱 COX-2 和 HIF-1α 水平的升高。这些结果为 CA 的药理作用及其在治疗肠道炎症方面的潜在用途提供了新的见解。
