Sencan A, Yilmaz O, Ozer E, Günşar C, Genç K, Ulukuş C, Taneli C, Mir E
Department of Pediatric Surgery, Celal Bayar University, Medical School, Manisa, Turkey.
Eur J Pediatr Surg. 2003 Aug;13(4):231-5. doi: 10.1055/s-2003-42235.
BACKGROUND/PURPOSE: We have shown in a previous study that sucralfate is beneficial in the prophylaxis and treatment of hypoxia/reoxygenation-induced intestinal injury. The aim of this study is to investigate whether sucralfate has any effect on the prevention of apoptosis in the ischemia/reperfusion (I/R)-induced intestinal injury.
Rats were randomized into three groups. Group 1 and 2 were subjected to I/R. Group 1 (treatment group) received sucralfate while group 2 (treatment control group) did not. Group 3 served as a normal control group (sham group). The terminal ileum was harvested for histopathologic investigation by light microscopy. The presence of apoptotic enterocytes (DNA fragmentation in cell nuclei) was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end-labeling (TUNEL) reaction.
In treatment control group, 3 of 7 rats had severe inflammation. None of the sucralfate-treated rats showed severe inflammation, 6 of them only showed mild inflammatory changes (p < 0.05). The apoptotic percentage was found to be 37.1 +/- 9.4 in the sucralfate-treated group (group 1), whereas it was 45.4 +/- 3.9 in the untreated group (group 2) (p < 0.05). The sham group had a completely normal intestinal architecture.
The present study shows that 1) the experimental model of I/R-induced intestinal injury induces enterocyte apoptosis; 2) sucralfate decreases enterocyte apoptosis in the experimental model of I/R-induced intestinal injury which may play a key role in the pathophysiological events leading to failure of the intrinsic gut barrier defense mechanisms.
背景/目的：我们在之前的一项研究中表明，硫糖铝对预防和治疗缺氧/复氧诱导的肠道损伤有益。本研究的目的是探讨硫糖铝对预防缺血/再灌注（I/R）诱导的肠道损伤中的细胞凋亡是否有任何作用。
将大鼠随机分为三组。第1组和第2组接受I/R处理。第1组（治疗组）给予硫糖铝，而第2组（治疗对照组）不给予。第3组作为正常对照组（假手术组）。取末端回肠进行光镜下的组织病理学检查。通过末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）反应检测凋亡肠上皮细胞（细胞核中的DNA片段化）的存在。
在治疗对照组中，7只大鼠中有3只出现严重炎症。接受硫糖铝治疗的大鼠均未出现严重炎症，其中6只仅表现出轻度炎症变化（p<0.05）。硫糖铝治疗组（第1组）的凋亡百分比为37.1±9.4，而未治疗组（第2组）为45.4±3.9（p<0.05）。假手术组的肠道结构完全正常。
本研究表明，1）I/R诱导的肠道损伤实验模型可诱导肠上皮细胞凋亡；2）硫糖铝可减少I/R诱导的肠道损伤实验模型中的肠上皮细胞凋亡，这可能在导致肠道固有屏障防御机制失效的病理生理事件中起关键作用。
