Kovács Tamás, Varga Gabriella, Erces Dániel, Tőkés Tünde, Tiszlavicz László, Ghyczy Miklós, Vécsei László, Boros Mihály, Kaszaki József
Szegedi Tudományegyetem, Általános Orvostudományi Kar Gyermekklinika, Gyermeksebészeti Osztály Szeged.
Magy Seb. 2012 Aug;65(4):191-7. doi: 10.1556/MaSeb.65.2012.4.4.
The consequence of inflammatory bowel diseases (IBD) is cytokine-mediated severe local tissue damage. Our aim was to determine the extent of inflammatory response and to influence the morphologic changes during the subacute phase of trinitro-benzene sulfonic acid (TNBS)-induced experimental colitis by oral phosphatidylcholine (PC) and N-methyl-D-aspartate (NMDA) receptor antagonist kynurenic acid therapy.
Sprague-Dawley rats were randomized to control, untreated colitis (ic TNBS), colitis fed with 2% PC-containing diet (3 days pre-treatment +3 days treatment after TNBS induction), colitis with kynurenic acid treatment (on day 6, n = 7) groups. The colitis was characterized by tissue myeloperoxidase and plasma TNF-alpha levels, the extent of tissue damage, structural changes in microvasculature (FITC-dextran staining) and mucosal injury (acridine orange staining) were determined by in vivo confocal laser scanning endomicroscopy (Optiscan Five1, Australia) and conventional histology (hematoxyilin-eosin staining).
Significant elevation in myeloperoxidase and TNF-alpha levels with remarkable damage in epithelial structure was detected in the colitis group. Both treatment regimens significantly decreased the level of inflammatory activation but only PC pretreatment could preserve the number of goblet cells and the epithelial structure. Treatment with kynurenic acid did not alter the morphology changes.
Oral PC pretreatment is a promising possibility in the therapy of IBDs through decreasing inflammatory reaction and increasing the number of goblet cells.
炎症性肠病（IBD）的后果是细胞因子介导的严重局部组织损伤。我们的目的是通过口服磷脂酰胆碱（PC）和N-甲基-D-天冬氨酸（NMDA）受体拮抗剂犬尿喹啉酸治疗，确定炎症反应的程度，并影响三硝基苯磺酸（TNBS）诱导的实验性结肠炎亚急性期的形态学变化。
将Sprague-Dawley大鼠随机分为对照组、未治疗的结肠炎组（经肠注射TNBS）、喂食含2%PC饮食的结肠炎组（TNBS诱导前预处理3天+诱导后治疗3天）、犬尿喹啉酸治疗的结肠炎组（第6天，n = 7）。通过组织髓过氧化物酶和血浆肿瘤坏死因子-α水平来表征结肠炎，通过体内共聚焦激光扫描内镜检查（澳大利亚Optiscan Five1）和传统组织学（苏木精-伊红染色）确定组织损伤程度、微血管结构变化（异硫氰酸荧光素-葡聚糖染色）和黏膜损伤（吖啶橙染色）。
在结肠炎组中检测到髓过氧化物酶和肿瘤坏死因子-α水平显著升高，上皮结构有明显损伤。两种治疗方案均显著降低了炎症激活水平，但只有PC预处理能够保留杯状细胞数量和上皮结构。犬尿喹啉酸治疗未改变形态学变化。
口服PC预处理通过减少炎症反应和增加杯状细胞数量，在IBD治疗中是一种有前景的方法。
