尽管有几种抗结肠炎药物可用，但它们的应用会带来许多副作用。菊苣酸 (CA) 是一种羟基肉桂酸，天然存在于菊苣 (Cichorium intybus)、紫锥菊 (Echinacea purpurea) 和罗勒中，具有多种健康益处，例如抗氧化和抗炎活性。在此，在大鼠中检查了 CA 对葡聚糖硫酸钠 (DSS) 诱导的大鼠结肠炎的潜在抗结肠炎功效。动物被随机分配到以下五组：对照组、CA（100 毫克/千克体重）、DSS [(DSS)； 4% w/v]、CA   DSS (100 mg/kg) 和 5-氨基水杨酸 (100 mg/kg)   DSS 组。获得的数据表明CA显着阻止结肠长度的缩短。同时，CA 使氧化应激相关酶增加，而丙二醛和一氧化氮显着减少。结果还表明，CA 给药显着降低了促凋亡指数（Bax 和 caspase-3），并显着增强了抗凋亡蛋白 Bcl-2。此外，DSS 还会导致促炎介质显着升高，包括白介素-1β、肿瘤坏死因子-α、髓过氧化物酶、环氧合酶 II、前列腺素 E2 和过氧化物酶体增殖物激活受体 γ。有趣的是，这些变化在 CA 管理后显着减少。在分子水平上，补充 CA 显着增加核因子红细胞 2 相关因子 2 (Nrf2) 的表达水平，并降低一氧化氮合酶和丝裂原激活蛋白激酶 14 的表达。 CA 已被确定可显着减少 DSS -通过激活Nrf2及其衍生的抗氧化剂分子并抑制与结肠炎发展相关的炎症和细胞凋亡级联来诱发结肠炎；表明 CA 可以用作替代的天然抗结肠炎药物。© 2023。作者获得 Springer-Verlag GmbH 德国（Springer Nature 旗下公司）的独家许可。

Although several anticolitic drugs are available, their application is associated with numerous side effects. Chicoric acid (CA) is a hydroxycinnamic acid found naturally in chicory (Cichorium intybus), purple coneflower (Echinacea purpurea), and basil with numerous health benefits, such as antioxidative and anti-inflammatory activities. Here, the potential anticolitic efficiency of CA against dextran sulfate sodium (DSS)-induced colitis in rats was examined in rats. Animals were randomly assigned to the following five groups: control, CA (100 mg/kg body weight), DSS [(DSS); 4% w/v], CA + DSS (100 mg/kg), and the 5-aminosalicylic acid (100 mg/kg) + DSS group. The obtained data revealed that CA significantly prevented the shortening of colon length. Meanwhile, the oxidative stress-related enzymes were increased, while malondialdehyde and nitric oxide, were markedly decreased significantly by CA. The results also indicated that CA administration decreased significantly the pro-apoptogenic indices (Bax and caspase-3) and enhanced significantly Bcl-2, the anti-apoptogenic protein. Moreover, DSS caused a significant elevation of pro-inflammatory mediators, including interleukin-1β, tumor necrosis factor-α, myeloperoxidase, cyclooxygenase II, prostaglandin E2, and peroxisome proliferator-activated receptor gamma. Interestingly, these changes were significantly decreased following the CA administration. At the molecular level, CA supplementation has increased significantly the expression level of nuclear factor erythroid 2-related factor-2 (Nrf2) and decreased the expressions of nitric oxide synthase and mitogen-activated protein kinase 14. CA has been determined to significantly lessen DSS-induced colitis by activating Nrf2 and its derived antioxidant molecules and suppressing inflammation and apoptosis cascades associated with the development of colitis; suggesting that CA could be used as an alternative naturally-derived anticolitic agent.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.