Mei Feng, Guo Sheng, He Yang-tao, Zhu Jiang, Zhou De-shan, Niu Jian-qin, Wang Han-zhi, Tian Yan-ping
Department of Histology and Embryology, Third Military Medical University, Chongqing 400038, China.
Virchows Arch. 2009 Apr;454(4):401-9. doi: 10.1007/s00428-009-0739-5. Epub 2009 Feb 12.
This study aimed at evaluating whether apoptosis of interstitial cells of Cajal (ICC), smooth muscle cells (SMC), and enteric neurons was involved in a guinea pig model of intestinal ischemia and reperfusion injury. The small intestinal segments were resected at either 6 (I60/R6h) and 12 h (I60/R12h) or 7 (I60/R7d) to 14 (I60/R14d) days after 60 min intestinal ischemia in the adult guinea pigs and studied by immunohistochemistry with anti-Kit, 5-bromo-2'-deoxyuridine (BrdU), alpha-smooth muscle actin, vimentin, and beta-tublin III antibodies. Also, apoptosis was tested by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. In the I60/R12h injury, there was a approximately 50% decrease of Kit+ cells in cell numbers at the level of myenteric plexus and a number of Kit-/vimentin-positive cells were labeled by TUNEL. Also, a few SMC and enteric neurons were TUNEL positive. The Kit+ ICC recovered to normal and a number of Kit-/BrdU-double-positive cells were observed in the I60/R14d group. Our results indicated that the intestinal I/R injury could lead to apoptosis of ICC, SMC, and enteric neurons which may contribute to the gastrointestinal motility disorders, and proliferation was involved in the recovery of ICC.
本研究旨在评估在豚鼠肠缺血再灌注损伤模型中, Cajal间质细胞(ICC)、平滑肌细胞(SMC)和肠神经元的凋亡是否与之相关。在成年豚鼠肠缺血60分钟后,于6小时(I60/R6h)和12小时(I60/R12h)或7天(I60/R7d)至14天(I60/R14d)切除小肠段,并用抗Kit、5-溴-2'-脱氧尿苷(BrdU)、α-平滑肌肌动蛋白、波形蛋白和β-微管蛋白III抗体进行免疫组织化学研究。此外,通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)法检测细胞凋亡。在I60/R12h损伤中,肌间神经丛水平的Kit+细胞数量减少约50%,许多Kit-/波形蛋白阳性细胞被TUNEL标记。此外,少数SMC和肠神经元TUNEL阳性。在I60/R14d组中,Kit+ ICC恢复正常,并观察到许多Kit-/BrdU双阳性细胞。我们的结果表明,肠缺血再灌注损伤可导致ICC、SMC和肠神经元凋亡,这可能导致胃肠动力障碍,而增殖参与了ICC的恢复。