大鼠肠缺血再灌注后肠黏膜细胞凋亡及GRP78表达的研究

发布时间：2018-08-05 09:56

【摘要】：目的：观察大鼠肠缺血再灌注损伤过程中肠黏膜的组织损伤和细胞凋亡及内质网分子伴侣葡萄糖调节蛋白78（Glucose regulated protein78kD, GRP78）的表达变化，探讨肠缺血再灌注损伤后肠黏膜细胞凋亡与内质网应激的可能机制。 方法：45只雄性SD大鼠随机分成9组:缺血再灌注0、1、3、6、12、24、48、72h组,以及假手术对照组,每组5只。实验组均夹闭大鼠的肠系膜上动脉1h后灌注，建立再灌注模型，假手术对照组仅游离肠系膜上动脉，不夹闭。然后采用HE染色观察肠黏膜变化，TUNEL法检测肠黏膜细胞凋亡，Western Blot和RT-PCR检测GRP78表达。 结果：缺血再灌注后，肠黏膜损伤程度及细胞凋亡指数随再灌注时间延长而增加，于再灌注3h达峰值（与其它组各组比较均P0.001），其后逐步减轻，于再灌注72h接近正常；缺血再灌注后，，GRP78的表达明显增加，于1h达第1个小高峰（与0h组和3h组比较P 0.05），但随再灌注时间的延长，表达量逐步减少，再灌注12h后开始回升（与6h组比较P 0.004），于24h达峰值（与其它各组比较均P 0.05），72h降至对照组水平（与假手术对照组比较P0.069）。 结论：肠缺血再灌注损伤启动内质网应激，而内质网应激通过某些途径诱导了肠黏膜细胞凋亡，且GRP78在大鼠肠缺血再灌注过程中表达变化，可能与其对肠缺血再灌注损伤保护机制有关。
[Abstract]:Aim: to observe the tissue damage and apoptosis of intestinal mucosa and the expression of endoplasmic reticulum molecular glucose regulatory protein 78 (Glucose regulated protein 78 KD, GRP78 during intestinal ischemia reperfusion injury in rats. To explore the possible mechanism of intestinal mucosal cell apoptosis and endoplasmic reticulum stress after intestinal ischemia reperfusion injury. Methods Forty-five male Sprague-Dawley rats were randomly divided into 9 groups: control group (n = 5) and sham operation group (n = 5). In the experimental group, the superior mesenteric artery was occluded for 1 hour, then the reperfusion model was established. In the sham operation control group, the superior mesenteric artery was only free and not clamped. Then HE staining was used to observe the changes of intestinal mucosa and Tunel method was used to detect the apoptosis of intestinal mucosal cells. Western Blot and RT-PCR were used to detect the expression of GRP78. Results: after ischemia-reperfusion, the degree of intestinal mucosal injury and apoptosis index increased with the prolongation of reperfusion time, and reached the peak at 3 h after reperfusion (compared with other groups, P0.001), then gradually reduced, and reached the normal level at 72 h after reperfusion. The expression of GRP78 increased significantly after ischemia reperfusion and reached the first peak at 1 h (P 0.05 compared with 0 h group and 3 h group), but decreased gradually with the prolongation of reperfusion time. After 12 hours of reperfusion, it began to rise (P 0.004 compared with 6h group), and reached its peak at 24 h (P 0.05 compared with other groups) and decreased to the control group at 72 h (P 0.069 compared with the sham operation control group). Conclusion: endoplasmic reticulum stress is initiated by intestinal ischemia-reperfusion injury, and endoplasmic reticulum stress induces intestinal mucosal cell apoptosis through some pathways, and the expression of GRP78 changes during intestinal ischemia-reperfusion injury in rats. It may be related to the protective mechanism of intestinal ischemia reperfusion injury.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R574

【参考文献】

相关期刊论文 前1条

1 胡国梁;何昆仑;范利;;内质网应激诱导的细胞凋亡与心肌缺血再灌注损伤[J];中华保健医学杂志;2010年01期

本文编号：2165433