摘要目的:运用坏死性小肠结肠炎(necrotizing enterocolitis, NEC)新生小鼠模型，探讨β-胡萝卜素对NEC新生小鼠肠道损伤的作用。方法:选用5日龄C57BL/6新生小鼠15只，按随机数字法分为三组，每组5只。对照组：母鼠哺乳喂养，无其他任何干预；NEC组：通过对新生小鼠缺氧刺激，人工喂养及脂多糖干预诱导产生NEC；β-胡萝卜素干预组：在诱导产生NEC的同时，给予新生小鼠胃管灌注β-胡萝卜素(1 mg/kg)。于生后第9日收集各组新生小鼠末端回肠组织，分析比较NEC病理评分，肠道炎症反应，肠上皮细胞增殖、凋亡及氧化应激水平。结果:与对照组相比，NEC组肠道出现明显损伤(0/5比5/5， P<0.05)，炎症反应(1.0122±0.03比9.5367±3.025， P<0.01)及氧化应激水平(TBARS 6.9292±0.129比11.4420±0.074， P<0.01; GPx 25.21±7.113比17.5674±5.769， P<0.01)明显升高，肠上皮细胞增殖能力下降(5.36±0.308比1.48±0.212， P<0.01)，且凋亡增多(2.5683±0.39比5.4974±0.967， P<0.01)；与NEC组相比，β-胡萝卜素干预组的肠道组织损伤程度明显降低(5/5比1/5， P<0.05)，肠道组织炎症减轻(9.5367±3.025比5.7871±1.489， P<0.01)，氧化应激水平明显下降(TBARS 11.4420±0.074比8.1148±0.013， P<0.01；GPx 17.5674±5.769比35.1576±11.077， P<0.01)，肠道上皮细胞增殖能力增强(1.48±0.212比3.8±0.1， P<0.01)，凋亡减少(5.4974±0.967比3.7773±0.772， P<0.05)；干预组肠道组织损伤程度及凋亡水平较NEC组有所改善的同时，与对照组比较差异无统计学意义( P>0.05)。 结论:β-胡萝卜素可通过降低肠道氧化应激水平来减轻NEC新生小鼠肠道损伤程度，缓解肠道炎症反应，促进肠上皮细胞增殖并抑制细胞凋亡。提示β-胡萝卜素对NEC新生小鼠肠道损伤具有保护作用。

abstractsObjective:To explore the function of β-carotene in a newborn murine model of necrotizing enterocolitis (NEC).Methods:A total of 15 five-day-old C57BL/6 mice were divided randomly into 3 groups ( n=5 each). Control group: neonatal mice were raised by adult mice; NEC group: mice were stimulated for NEC modeling by oxygen deficit, artificial feeding and lipopolysaccharide (LPS) intervention; β-carotene intervention group: apart from stimuli of NEC modeling, 1 mg/kg body weight β-carotene was given daily to neonatal mice. At Day 9 after birth, terminal ileum tissues of neonatal mice were harvested and pathological scores, inflammation level, enterocyte proliferation, apoptosis and oxidative stress level were estimated. Results:As compared to control group, apparent injury (0/5 vs. 5/5, P<0.05), high level of inflammation (1.0122±0.03 vs. 9.5367±3.025, P<0.01) and oxidative stress (TBARS 6.9292±0.129 vs. 11.4420±0.074, P<0.01; GPx 25.21±7.113 vs. 17.5674±5.769, P<0.01), lower proliferation ( P<0.01) and more apoptotic cells were found in NEC group ( P<0.01); while in β-carotene intervention group, relative to NEC group, injury grade (5/5 vs. 1/5, P<0.05), inflammation (9.5367±3.025 vs. 5.7871±1.489, P<0.01) and oxidative stress level (TBARS 11.4420±0.074 vs. 8.1148±0.013, P<0.01; GPx 17.5674±5.769 vs. 35.1576±11.077, P<0.01) and apoptotic cells declined (5.4974±0.967 vs. 3.7773±0.772, P<0.05), but on the contrary, proliferative capability of intestine improved apparently (1.48±0.212 vs. 3.8±0.1, P<0.01). In addition, compared with control group, no significant difference existed in the level of intestinal tissue injury or apoptosis in β -carotene intervention group ( P>0.05). Conclusions:β-carotene can alleviate the intestinal damage of NEC newborn mice by reducing the level of intestinal oxidative stress and inflammation, promoting intestinal epithelial cell proliferation and inhibiting apoptosis. It hints that β-carotene has a protective effect upon intestinal injury of NEC newborn mice.