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成年豚鼠肠道缺血再灌注损伤诱导的 Cajal 间质细胞、平滑肌细胞和肠神经元凋亡

Apoptosis of interstitial cells of Cajal, smooth muscle cells, and enteric neurons induced by intestinal ischemia and reperfusion injury in adult guinea pigs.

作者信息

Mei Feng, Guo Sheng, He Yang-tao, Zhu Jiang, Zhou De-shan, Niu Jian-qin, Wang Han-zhi, Tian Yan-ping

机构信息

Department of Histology and Embryology, Third Military Medical University, Chongqing 400038, China.

出版信息

Virchows Arch. 2009 Apr;454(4):401-9. doi: 10.1007/s00428-009-0739-5. Epub 2009 Feb 12.

Abstract

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.

摘要

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。

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