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目的探讨甘氨酸对内毒素和缺氧诱导的坏死性肠炎(NEC)鼠血清炎性因子IL-1与IL-6的作用.方法 40只SD大鼠随机分为甘氨酸+LPS组和NS+LPS对照组.甘氨酸组大鼠静脉给予甘氨酸1 g/kg,5 min后给予内毒素2 mg/kg,NS对照组用等量的生理盐水代替甘氨酸,内毒素剂量同前.所有大鼠注射LPS 90 min后氧吸入浓度从21%降至5%,继续机械通气至鼠死亡或存?80 min,实验结束时采血样和小肠标本.用双抗夹心ELISA法测定血清IL-1与IL-6的含量,肠组织做病理检查并进行NEC分度.结果甘氨酸组的存活时间(159.25±22.78) min长于NS对照组(138.75±19.05) min,差异有显著性(P<0.01).甘氨酸组小肠病理损伤程度明显明显低对照组(P<0.01).甘氨酸组血清IL-1的含量为(149.1±76.1) ng/L,显著低于对照组(472.1±505.6) ng/L(P<0.01);血清IL-6的含量为(204.8±163.5) ng/L,亦显著低于对照组(585.8±574.5) ng/L(P<0.01).结论甘氨酸可降低内毒素和缺氧诱导的坏死性肠炎(NEC)鼠血清IL-1和IL-6含量水平,减轻肠病理损伤.“,”Objective To explore the effect of glycine on serum levels of IL-1 and IL-6 in rats with necrotizing enterocolitis (NEC) induced by endotoxin and hypoxia. Methods Forty SD rats were randomly assigned into the glycine-treated group and the normal saline (NS) control group. In the glycine-treated group, glycine (1 g/kg) was injected intravenously and lipopolysaccharide (LPS) of 2 mg/kg was administrated five minutes later. The control group rats were treated with the same volume of NS as a substitute for glycine. In both groups, 90 minutes after injection of LPS, FiO2 given was reduced from 21% to 5% and ventilation continued for 180 min or until the death of rats. At the end of the experiment, the blood samples and sections of the intestine were obtained immediately. Serum levels of IL-1 and IL-6 were measured using ELISA. The histopathological changes of the small intestine were studied. Results The survival time of the glycine-treated group was significantly longer than that of the control group [(159.25±22.78) min vs (138.75±19.05) min](P<0.01). The injury of the small intestine in the glycine-treated group was markedly alleviated (P<0.01). The levels of IL-1and IL-6 in the glycine-treated group were significantly lower than those in the control group [(149.1±76.1) ng/L vs (472.1±505.6) ng/L, (204.8±163.5) ng/L vs (585.8±574.5) ng/L, respectively] (P<0.01). Conclusions Glycine could reduce the levels of IL-1 and IL-6 and alleviate injuries of the intestine in rats with NEC induced by LPS and hypoxia.