Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Inflammopharmacology. 2019 Dec;27(6):1265-1273. doi: 10.1007/s10787-019-00581-w. Epub 2019 Mar 28.
Pathogenesis of the inflammatory bowel disease (IBD) involves the combination of immunological and inflammatory factors. IBD is associated with several extra-intestinal manifestations. The exact underlying bridge between the probable cardiac diseases in IBD patients is undetermined. Trigonelline is an alkaloid with several therapeutic potential properties. In this study, we aimed to assess the probable underlying mechanisms of this comorbidity as well as protective effect of trigonelline focusing inflammatory response and oxidative state in mouse model of colitis. Dextran sodium sulfate (DSS) was used for induction of colitis in mice. Trigonelline (10, 50 and 100 mg/kg) was administrated via intraperitoneal rout (i.p.) for 14 continuous days. Heart, intestine and serum samples were taken for assessment of total antioxidant capacity, malondialdehyde (MDA), gene expressions of inflammatory markers including tumor necrosis factor alpha (Tnf-α), interleukin 1-beta (Il/1β), toll- like receptor 4 (Tlr4) as well as for evaluation of histopathological alterations. Results demonstrated that trigonelline effectively attenuated the cellular/molecular and histopathological adverse effects of colitis in the intestine and heart tissues. In this regards, we found that trigonelline decreased the MDA level, attenuated the expression of Tnf-α, Il/1β and, Tlr4 as well as modulated the histopathological alterations in the intestine. Furthermore, trigonelline increased the antioxidant capacity in the related experimental groups. We concluded that IBD (colitis) is associated with comorbid cellular/molecular modifications in the heart and for the first time, we found that trigonelline has potential therapeutic effects (at least partially) to attenuate the cardiac manifestations of the colitis.
炎症性肠病（IBD）的发病机制涉及免疫和炎症因素的结合。IBD 与几种肠外表现有关。IBD 患者可能存在的心脏疾病之间的确切潜在联系尚不清楚。六氢吡啶是一种具有多种治疗潜力的生物碱。在这项研究中，我们旨在评估这种合并症的潜在潜在机制以及六氢吡啶对结肠炎小鼠模型中炎症反应和氧化状态的保护作用。葡聚糖硫酸钠（DSS）用于诱导小鼠结肠炎。六氢吡啶（10、50 和 100mg/kg）通过腹腔途径（i.p.）连续 14 天给药。采集心脏、肠道和血清样本，评估总抗氧化能力、丙二醛（MDA）、炎症标志物包括肿瘤坏死因子-α（Tnf-α）、白细胞介素 1-β（Il/1β）、toll-样受体 4（Tlr4）的基因表达，以及评估组织病理学改变。结果表明，六氢吡啶有效减轻了肠道和心脏组织中结肠炎的细胞/分子和组织病理学不良影响。在这方面，我们发现六氢吡啶降低了 MDA 水平，减弱了 Tnf-α、Il/1β 和 Tlr4 的表达，并调节了肠道的组织病理学改变。此外，六氢吡啶增加了相关实验组的抗氧化能力。我们得出结论，IBD（结肠炎）与心脏的合并症细胞/分子改变有关，这是我们首次发现六氢吡啶具有潜在的治疗效果（至少部分）来减轻结肠炎的心脏表现。
