Ulcerative colitis (UC) is an intractable ailment, in which may chronic inflammations/ulcerations may develop in the mucosal lining of the colon with multiple recurrences. Various drugs such as steroids, immunosuppressants, and antibiotics are extensively used to treat UC. The patients suffer from adverse effects of these advanced drugs. So, they need a harmless therapeutic agent from natural sources. The therapeutic D-carvone has an anti-inflammatory action against the investigational colon cancer models. Therefore, we analyzed the effect of D-carvone on dextran sulfate sodium (DSS) provoked colitis model in mice as follows: Group I: noncolitis healthy control mice; Group II: ulcerative colitis mice models; Group III: D-carvone (40 mg/kg) + ulcerative colitis models; Group IV: sulfasalazine (50 mg/kg) + ulcerative colitis models. On the 8th day, the experimental study was terminated and serum samples and colon tissues were processed for further analysis. The effect of D-carvone at different concentration was studied on the LPS challenged RAW 264.7 cell lines. The D-carvone (40 mg/kg) treatment maintained the colon length and decreased disease activity index (DAI) score in UC animals. The increased antioxidant enzymes status and decreased oxidative stress and pro-inflammatory markers were noted in the D-carvone (40 mg/ kg) + UC mice. Histopathological study of colon tissue of D-carvone (40 mg/kg) treated UC mice displayed less mucosal damage and improved crypt integrity and goblet cells compared with DSS only provoked mice. The im-munohistochemical expression of iNOS and COX-2 was drastically diminished in the D-carvone treated UC mice. D-carvone (40 mg/kg) treatment appreciably diminished the LPS provoked NO production and pro-inflammatory modulators in the RAW 264.7 macrophage cell lines. These findings proved that D-carvone has a potential therapeutic effect to prevent LPS induced inflammation in in vitro cells and chemically induced ulcerative colitis in vivo models.

中文翻译：

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D-香芹酮通过抑制COX-2和TNF-α对Balb / c小鼠和LPS诱导的RAW细胞对右旋糖酐硫酸钠诱导的溃疡性结肠炎的保护作用。

溃疡性结肠炎（UC）是一种顽固的疾病，其中结肠的粘膜内层可能会发生慢性炎症/溃疡，并多次复发。各种药物，例如类固醇，免疫抑制剂和抗生素，被广泛用于治疗UC。患者遭受这些先进药物的不良反应。因此，他们需要天然来源的无害治疗剂。治疗性D-香芹酮对结肠癌模型具有抗炎作用。因此，我们分析了D-香芹酮对小鼠右旋糖酐硫酸钠（DSS）诱发的结肠炎模型的作用，如下：第一组：非结肠炎健康对照小鼠；第二组：溃疡性结肠炎小鼠模型；第三组：D-香芹酮（40 mg / kg）+溃疡性结肠炎模型；第四组：柳氮磺吡啶（50 mg / kg）+溃疡性结肠炎模型。在第8天，实验研究终止，血清样品和结肠组织被处理以进行进一步分析。研究了不同浓度的D-香芹酮对LPS攻击的RAW 264.7细胞系的影响。D-香芹酮（40 mg / kg）处理可维持UC动物的结肠长度，并降低疾病活动指数（DAI）评分。在D-香芹酮（40 mg / kg）+ UC小鼠中发现抗氧化酶状态增加，氧化应激和促炎性标志物降低。与仅DSS刺激的小鼠相比，D-香芹酮（40 mg / kg）处理的UC小鼠结肠组织的组织病理学研究显示较少的粘膜损伤，并改善了隐窝完整性和杯状细胞。在经D-香芹酮处理的UC小鼠中，iNOS和COX-2的免疫组织化学表达大大降低。D-香芹酮（40 mg / kg）处理可明显减少RAW 264.7巨噬细胞系中LPS引起的NO产生和促炎性调节剂。这些发现证明D-香芹酮具有预防LPS诱导的炎症的潜在治疗作用。体外细胞和化学诱导的溃疡性结肠炎的体内模型。