Department of Cardiovascular and Neurologic Disease (Stroke Center), College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Department of Pharmaceutical Biochemistry, College of Pharmacy, Kyung Hee University, Seoul 02447, Korea.
Nutrients. 2020 Feb 12;12(2):456. doi: 10.3390/nu12020456.
Inflammatory bowel disease (IBD) is a major risk factor of colorectal cancer. Drugs currently used for IBD exhibit adverse effects including vomiting, nausea, and diarrhea. Naturally derived novel alternative therapies are required to overcome these limitations. In this study, we investigated the protective effects of ethanol extract of (CEE) in a dextran sodium sulfate (DSS)-induced mouse model of colitis. CEE markedly improved DSS-induced clinical symptoms and histological status, such as the disease activity index, spleen weight, and colon length. Moreover, CEE-treated mice showed significant recovery of DSS-induced crypt damage and cell death. CEE suppressed myeloperoxidase (MPO) activity and macrophage marker F4/80 mRNA expression in colonic tissue of mice with DSS-induced colitis, indicating neutrophil infiltration and macrophage accumulation, respectively. Although DSS upregulated pro-inflammatory mediators and activated transcription factors, CEE downregulated the mRNA expression of cytokines including interleukin-6, interleukin-1β, and tumor necrosis factor-α, protein expression of cyclooxygenase-2 and inducible nitric oxide synthase, as well as activation of nuclear factor-kappa B (NF-кB) and signal transducer and activator of transcription 3 (STAT3). Hence, our findings reveal that the anti-inflammatory properties of CEE, involving the downregulation of the expression of pro-inflammatory mediators by inactivating NF-кB and STAT3 in DSS-induced colitis mice.
炎症性肠病（IBD）是结直肠癌的一个主要危险因素。目前用于治疗 IBD 的药物存在呕吐、恶心和腹泻等不良反应。需要寻找新型的天然衍生替代疗法来克服这些局限性。在这项研究中，我们研究了 （CEE）在葡聚糖硫酸钠（DSS）诱导的结肠炎小鼠模型中的保护作用。CEE 显著改善了 DSS 诱导的临床症状和组织学状态，如疾病活动指数、脾脏重量和结肠长度。此外，CEE 治疗的小鼠显示出 DSS 诱导的隐窝损伤和细胞死亡的显著恢复。CEE 抑制了 DSS 诱导的结肠炎小鼠结肠组织中的髓过氧化物酶（MPO）活性和巨噬细胞标志物 F4/80mRNA 表达，分别表明中性粒细胞浸润和巨噬细胞聚集。虽然 DSS 上调了促炎介质和激活了转录因子，但 CEE 下调了包括白细胞介素-6、白细胞介素-1β和肿瘤坏死因子-α在内的细胞因子的 mRNA 表达、环氧化酶-2 和诱导型一氧化氮合酶的蛋白表达，以及核因子-kappa B（NF-кB）和信号转导和转录激活因子 3（STAT3）的激活。因此，我们的研究结果表明，CEE 的抗炎特性涉及通过使 DSS 诱导的结肠炎小鼠中的 NF-кB 和 STAT3 失活来下调促炎介质的表达。
