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Characterization of apoptosis in intestinal ischaemia-reperfusion injury — a light and electron microscopic study.

机译:肠缺血再灌注损伤中细胞凋亡的特征-光和电镜研究。

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摘要

Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline (n = 6) or modified University of Wisconsin solution (n = 6) at 4 °C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury.
机译:肠缺血再灌注(IR)损伤主要归因于细胞坏死。细胞凋亡后,IR照射到大脑,心脏,肾上腺和肾脏后,观察到了一种独特的细胞死亡形式。为了表征细胞凋亡在肠道IR中的作用,将小肠移植物在生理盐水(n = 6)或改良的威斯康星大学溶液(n = 6)中于4 C储存12 h,然后在同系大鼠中再灌注6 h 。通过光镜和电子显微镜分析正常,储存和再灌注后1、3、6 h的肠道样品。再灌注后,有隐窝和绒毛上皮细胞凋亡,隐窝和绒毛结构丧失以及粘膜炎性细胞浸润增加。持续的凋亡在1 h达到最大,其程度随着再灌注间隔的增加而降低。从再灌注3小时开始,大量凋亡小体占据了主导地位。这项研究证明了肠道IR损伤诱导的细胞凋亡,这在再灌注后一小时内开始,可能是所观察到的隐窝和绒毛损失的原因。与坏死相反,这具有潜在的治疗意义,凋亡是遗传调节剂和生化效应子的活跃过程,可以专门针对预防或减轻IR损伤。

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