论文部分内容阅读
本研究采用大鼠胃缺血-再灌注(gastric ischemia-reperfusion,GI-R)模型(夹闭腹腔动脉30min后再灌注),通过组织学免疫组化等方法,研究GI-R不同时间(0、0．5、1、3、6、24、48、72 h)对胃黏膜细胞凋亡和增殖的影响。结果发现,单纯缺血30min胃黏膜损伤较轻,再灌注后损伤逐渐加重,胃黏膜的凋亡细胞迅速增加,而增殖细胞迅速减少：至再灌注后1h达高峰；之后胃黏膜开始修复,凋亡细胞逐渐减少,增殖细胞逐渐增加：至再灌注后24h胃黏膜细胞增殖达高峰；再灌注后72h胃黏膜基本恢复正常。上述结果提示,在GI-R中,胃黏膜损伤主要由再灌注引起,凋亡细胞增加；然后胃黏膜启动自我修复机制,增殖细胞逐渐取代损伤细胞,3d左右就可基本修复,表明胃黏膜细胞具有很强的自我修复能力。
In this study, GI-R model (occlusion of celiac artery 30 min after reperfusion) was used to study the effect of GI-R on the ischemia-reperfusion (GI-R) , 0.5,1,3,6,24,48,72 h) on gastric mucosal cell apoptosis and proliferation. The results showed that gastric mucosa lesion was mild after 30min ischemia, and the injury gradually increased after reperfusion. The number of apoptotic cells in gastric mucosa increased rapidly and the number of proliferating cells decreased rapidly: the peak was reached at 1h after reperfusion, and then the gastric mucosa began to repair. The number of apoptotic cells gradually decreased and the number of proliferating cells increased gradually. The proliferation of gastric mucosa reached a peak at 24h after reperfusion, and gastric mucosa returned to normal at 72h after reperfusion. The above results suggest that, in GI-R, gastric mucosal injury is mainly caused by reperfusion, and apoptotic cells increase; then gastric mucosa initiates a self-repair mechanism, proliferative cells gradually replace damaged cells and can be basically restored after about 3d, indicating that gastric mucosal cells Has a strong self-healing ability.