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目的 :探索甘氨酸对抗内毒素和缺氧所诱导鼠坏死性肠炎 (NEC)的作用。方法 :以SD大鼠为实验动物 ,给予麻醉和机械通气。试验组 2 0只经静脉给予甘氨酸 ,5min后给脂多糖 ,对照组用等量的生理盐水代替甘氨酸。所有大鼠 90min后吸入浓度从 2 1%降至 5 %的氧 ,继续机械通气至鼠死亡或存活 180min ,采血样和小肠标本进行检查。用ELISA法测血清TNF -α ,硝酸还原酶法测NO ,肠组织作病理检查并进行NEC分度。结果 :两组的存活时间为甘氨酸组 (15 9 2 5± 2 2 78)min与对照组 (138 75± 19 0 5 )min ,差异显著 (P <0 0 1)。甘氨酸组小肠病理损伤程度明显轻于对照组 (P <0 0 1)。血清TNF -α的含量水平甘氨酸组为 (12 0 74± 47 2 2 )ng/L ,显著低于对照组的(2 2 0 2 3± 90 35 )ng/L(P <0 0 1)。血清NO的含量水平甘氨酸组为 (15 2 96± 6 5 5 3) μmol/L ,明显低于对照组的(2 2 7 19± 10 4 11) μmol/L (P <0 0 5 )。 结论 :甘氨酸能降低脂多糖和缺氧诱导的NEC鼠血清TNF -α和过量的NO的含量水平 ,减轻肠病理损伤。
Objective: To explore the role of glycine against endotoxin and hypoxia induced rat necrotic enteritis (NEC). Methods: SD rats were used as experimental animals and anesthetized and mechanically ventilated. In the experimental group, 20 rabbits were given intravenous glycine, 5 minutes later, lipopolysaccharide was given to the experimental group, and the control group was given saline instead of glycine. After 90mins inhalation, the concentration of oxygen was reduced from 21% to 5% oxygen in all rats. Mechanical ventilation was continued until the mice died or survived for 180min. Blood samples and small intestine samples were inspected. Serum TNF-α was detected by ELISA, nitric acid reductase was measured NO, intestinal tissue for pathological examination and NEC index. Results: The survival time of the two groups was significantly different between the glycine group (15 925 +/- 2278) min and the control group (138 75 +/- 19 05) min (P <0.01). Glycine group of intestinal pathological damage was significantly lighter than the control group (P <0.01). Serum levels of TNF-αin the glycine group were (12 0 74 ± 47 2 2) ng / L, which were significantly lower than those in the control group (2 023 ± 90 35) ng / L (P 0 01). The levels of serum NO in glycine group were (15 2 96 ± 6 5 5 3) μmol / L, which were significantly lower than those in control group (2 2 7 19 ± 10 4 11) μmol / L (P 0 05). CONCLUSION: Glycine can reduce the levels of serum TNF-α and excessive NO in lipopolysaccharide and hypoxia-induced NEC rats and reduce the pathological damage of intestinal tract.