Triantafillidis John K, Douvi Georgia, Agrogiannis George, Patsouris Efstratios, Gikas Aristofanis, Papalois Apostolos E
Inflammatory Bowel Disease Unit, IASO General Hospital, 264 Mesogeion Avenue, Holargos, 15562 Athens, Greece.
1st Department of Pathology, University of Athens, School of Medicine, 75 Mikras Asias, 115 27 Athens, Greece.
Biomed Res Int. 2014;2014:648535. doi: 10.1155/2014/648535. Epub 2014 May 4.
Experimental data suggest that oral iron (I.) supplementation can worsen colitis in animals.
To investigate the influence of various concentrations of orally administered I. in normal gut mucosa and mucosa of animals with TNBS colitis, as well as the influence of Mesalamine (M.) and Prednisolone (P.) on the severity of TNBS colitis following orally administered I.
156 Wistar rats were allocated into 10 groups. Colitis was induced by TNBS. On the 8th day, all animals were euthanatized. Activity of colitis and extent of tissue damage were assessed histologically. The levels of tissue tumor necrosis factor- α (t-TNF- α ) and tissue malondialdehyde (t-MDA) were estimated in all animal groups.
Moderate and high I. supplementation induced inflammation in the healthy colon and increased the activity of the experimentally induced TNBS colitis. Administration of M. on TNBS colitis following moderate iron supplementation (0.3 g/Kg diet) resulted in a significant improvement in the overall histological score as well as in two individual histological parameters. M. administration, however, did not significantly reduce the t-TNF- α levels (17.67 ± 4.92 versus 14.58 ± 5.71, P = 0.102), although it significantly reduced the t-MDA levels (5.79 ± 1.55 versus 3.67 ± 1.39, P = 0.000). Administration of M. on TNBS colitis following high iron supplementation (3.0 g/Kg diet) did not improve the overall histological score and the individual histological parameters, neither reduced the levels of t-TNF- α (16.57 ± 5.61 versus 14.65 ± 3.88, P = 0.296). However, M. significantly reduced the t-MDA levels (5.99 ± 1.37 versus 4.04 ± 1.41, P = 0.000). Administration of P. on TNBS colitis after moderate iron supplementation resulted in a significant improvement in the overall histological score as well as in three individual histological parameters. P. also resulted in a significant reduction in the t-TNF- α levels (17.67 ± 4.92 versus 12.64 ± 3.97, P = 0.003) and the t-MDA levels (5.79 ± 1.54 versus 3.47 ± 1.21, P = 0.001). Administration of P on TNBS colitis after high I. supplementation resulted in a significant improvement of the overall histological score and three individual histological parameters and significantly reduced the levels of t-TNF- α (16.6 ± 5.6 versus 11.85 ± 1.3, P = 0.001).
I. can induce colonic inflammation and aggravate TNBS colitis. M. and P. can significantly improve the inflammatory process in the colonic mucosa in TNBS colitis aggravated by orally administered I. P. has a stable anti-TNF- α effect. These findings suggest that the harmful.
实验数据表明，口服补充铁剂可使动物结肠炎病情恶化。
研究不同浓度口服铁剂对正常肠道黏膜以及三硝基苯磺酸（TNBS）诱导的结肠炎动物黏膜的影响，以及美沙拉嗪（M）和泼尼松龙（P）对口服铁剂后TNBS结肠炎严重程度的影响。
将156只Wistar大鼠分为10组。用TNBS诱导结肠炎。第8天，对所有动物实施安乐死。通过组织学评估结肠炎的活动度和组织损伤程度。测定所有动物组的组织肿瘤坏死因子-α（t-TNF-α）水平和组织丙二醛（t-MDA）水平。
中等剂量和高剂量补充铁剂可诱发健康结肠炎症，并增加实验性诱导的TNBS结肠炎的活动度。在中等剂量铁剂补充（0.3 g/Kg饮食）后给予M治疗TNBS结肠炎，可使总体组织学评分以及两个个体组织学参数得到显著改善。然而，给予M虽然显著降低了t-MDA水平（5.79±1.55对3.67±1.39，P = 0.000），但并未显著降低t-TNF-α水平（17.67±4.92对14.58±5.71，P = 0.102）。在高剂量铁剂补充（3.0 g/Kg饮食）后给予M治疗TNBS结肠炎，既未改善总体组织学评分和个体组织学参数，也未降低t-TNF-α水平（16.57±5.61对14.65±3.88，P = 0.296）。然而，M显著降低了t-MDA水平（5.99±1.37对4.04±1.41，P = 0.000）。中等剂量铁剂补充后给予P治疗TNBS结肠炎，可使总体组织学评分以及三个个体组织学参数得到显著改善。P还可使t-TNF-α水平（17.67±4.92对12.64±3.97，P = 0.003）和t-MDA水平（5.79±1.54对3.47±1.21，P = 0.001）显著降低。高剂量铁剂补充后给予P治疗TNBS结肠炎，可使总体组织学评分和三个个体组织学参数得到显著改善，并显著降低t-TNF-α水平（16.6±5.6对11.85±1.3，P = 0.001）。
铁剂可诱发结肠炎症并加重TNBS结肠炎。M和P可显著改善口服铁剂加重的TNBS结肠炎中结肠黏膜的炎症过程。P具有稳定的抗TNF-α作用。这些发现提示有害性。
