Chira Alexandra, Braicu Cornelia, Budisan Liviuta, Ioan Chira Romeo, Berindan-Neagoe Ioana, Lucian Dumitrascu Dan
Second Medical Clinic, Department of Internal Medicine, 'Iuliu Hatieganu' University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania.
Research Center for Functional Genomics, Biomedicine and Translational Medicine, 'Iuliu Hatieganu' University of Medicine and Pharmacy, 400337 Cluj-Napoca, Romania.
Exp Ther Med. 2020 Jul;20(1):24-30. doi: 10.3892/etm.2020.8665. Epub 2020 Apr 15.
Irritable bowel syndrome (IBS) is one the most frequent and common functional gastrointestinal disorders that has a multifactorial etiopathogenesis. Multiple biomarkers have been tested in search for a reliable and specific biomarker, but there is not yet a specific biomarker for IBS. The aim of this study was to evaluate two biomarkers of different putative pathways of the pathogenesis of IBS: the monocyte chemotactic protein-1 (MCP-1) and nitrotyrosine, in order to establish their role as potential biomarkers. We enrolled 42 consecutive IBS patients diagnosed by Rome III criteria and 35 consecutive healthy controls. Serum concentrations for the two biomarkers (MCP-1 and nitrotyrosine) were determined using commercial ELISA kits. Serum levels of MCP-1 were not statistically significantly higher in IBS patients than in controls (204±130 vs. 174±73 pg/ml; P=0.311). Nitrotyrosine levels were statistically significantly lower in IBS patients than in controls (30±12 vs. 353±14 nM; P=0.050). MCP-1 levels were higher in IBS patients with metabolic syndrome versus IBS patients without metabolic syndrome (239±153 vs. 168±120 pg/ml; P=0.948) and in controls with metabolic syndrome (174±56 pg/ml). MCP-1 serum levels were statistically significantly higher in IBS patients with metabolic syndrome than in controls (239±153 vs. 157±89 pg/ml; P=0.037), suggesting multiple factors being involved, particularly the diet and its relation with the metabolic syndrome, and it suggests that MCP-1 could be a marker of subclinical atherosclerosis. Low-grade inflammation might be related to oxidative stress, which plays an underestimated role in the pathogenesis of IBS.
肠易激综合征（IBS）是最常见的功能性胃肠疾病之一，其发病机制具有多因素性。人们已经对多种生物标志物进行了测试，以寻找可靠且特异的生物标志物，但目前仍没有针对IBS的特异性生物标志物。本研究的目的是评估IBS发病机制中不同假定途径的两种生物标志物：单核细胞趋化蛋白-1（MCP-1）和硝基酪氨酸，以确定它们作为潜在生物标志物的作用。我们纳入了42例根据罗马III标准诊断的连续性IBS患者和35例连续性健康对照。使用商用ELISA试剂盒测定两种生物标志物（MCP-1和硝基酪氨酸）的血清浓度。IBS患者的MCP-1血清水平在统计学上并不显著高于对照组（204±130 vs. 174±73 pg/ml；P=0.311）。IBS患者的硝基酪氨酸水平在统计学上显著低于对照组（30±12 vs. 353±14 nM；P=0.050）。患有代谢综合征的IBS患者的MCP-1水平高于未患代谢综合征的IBS患者（239±153 vs. 168±120 pg/ml；P=0.948），在患有代谢综合征的对照组中为（174±56 pg/ml）。患有代谢综合征的IBS患者的MCP-1血清水平在统计学上显著高于对照组（239±153 vs. 157±89 pg/ml；P=0.037），这表明涉及多种因素，特别是饮食及其与代谢综合征的关系，并且表明MCP-1可能是亚临床动脉粥样硬化的标志物。低度炎症可能与氧化应激有关，氧化应激在IBS的发病机制中起着被低估的作用。
