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目的动态观察新生大鼠坏死性小肠结肠炎(NEC)发病过程中肠细胞凋亡率变化及其与肠损伤关系。方法40只新生SD大鼠随机分成对照组(C)和模型组(M)。对照组8只;模型组32只,在出生48h开始给予鼠配方奶人工喂养,100%氮气缺氧90s,4℃冷刺激10min,每天2次,连续3d,建立新生大鼠NEC模型;模型组开始造模后24h(M24)、48h(M48)、72h(造模结束,M72)及造模结束后24h(M96)分别处死8只,留取肠管进行肠组织损伤评分和肠细胞凋亡率检测(流式细胞仪)。组织学评分≥2确定为NEC。各组随机选取1份回盲部近端小肠标本进行肠黏膜透射电镜检查。采用SPSS11.0统计学软件进行统计分析,α=0.05为显著性检验标准。结果透射电镜显示模型组大鼠肠黏膜出现大量凋亡细胞,形成凋亡小体。对照组、M24、M48、M72和M96肠组织损伤评分分别为(0.08±0.15)、(1.38±0.42)、(1.46±0.69)、(1.58±0.30)分和(3.33±0.59)分,肠细胞凋亡率分别为4.8%±2.9%、12.8%±6.3%、14.9%±5.5%、17.7%±5.5%和27.6%±9.9%。肠损伤程度与肠细胞凋亡率呈显著正相关(r凋亡率=0.853,P<0.01)。结论新生鼠肠细胞凋亡增加是NEC肠组织损伤起始事件;随时间延长,肠细胞凋亡增加程度进一步加重;肠细胞凋亡增加是造成新生鼠NEC肠道进行性损伤的病理基础。
Objective To observe the changes of apoptosis rate of intestinal cells and the relationship with intestinal injury in neonatal rats with necrotizing enterocolitis (NEC). Methods 40 newborn SD rats were randomly divided into control group (C) and model group (M). The rats in model group (n = 32) were fed with artificial milk formula at 48 hours after birth, hypoxia 90% at 100% nitrogen, cold stimulation at 4 ℃ for 10 minutes, twice daily for 3 days. Eight mice were sacrificed 24h (M24), 48h (M48), 72h (at the end of modeling, M72) and 24 h after modeling (M96) respectively. Intestinal tissues were sacrificed for bowel injury score and enterocyte apoptosis rate Detection (flow cytometry). Histological score ≥ 2 was determined as NEC. Each group randomly selected 1 ileocecal proximal intestinal specimens for intestinal mucosa transmission electron microscopy. Using SPSS11.0 statistical software for statistical analysis, α = 0.05 for the significance test. Results Transmission electron microscopy revealed a large number of apoptotic cells in the intestinal mucosa of rats in model group, forming apoptotic bodies. The scores of intestinal injury in M24, M48, M72 and M96 were (0.08 ± 0.15), (1.38 ± 0.42), (1.46 ± 0.69), (1.58 ± 0.30) and (3.33 ± 0.59) The apoptotic rates were 4.8% ± 2.9%, 12.8% ± 6.3%, 14.9% ± 5.5%, 17.7% ± 5.5% and 27.6% ± 9.9%, respectively. Intestinal damage and intestinal cell apoptosis rate was significantly correlated (r rate of apoptosis = 0.853, P <0.01). Conclusions The increase of apoptosis of intestinal cells in neonatal rats is the initiating event of intestinal tissue injury of NEC. With the prolongation of time, the increase of apoptosis of intestinal cells further aggravates; the increase of intestinal cell apoptosis is the pathological basis of intestinal injury induced by NEC in neonatal rats.