甘氨酸对脂多糖和缺氧诱导鼠坏死性肠炎的影响

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20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21%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(159.25±22.78)min与对照组(138.75±19.05)min,差异显著(P＜0.01)。甘氨酸组小肠病理损伤程度明显轻于对照组(P＜0.01)。血清TNF-α的含量水平甘氨酸组为(120.74±47.22)ng/L,显著低于对照组的(220.23±90.35)ng/L(P＜0.01)。血清NO的含量水平甘氨酸组为(152.96±65.53)μmol/L,明显低于对照组的(227.19±104.11)μmol/L(P＜0.05)。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。

Effect of glycine on lipopolysaccharide and hypoxia-induced necrotizing enterocolitis in rats

AIM:To investigate the effect of glycine on endotoxin and hypoxia-induced necrotizing exterocolitos (NEC) in rats. METHODS:In glycine+NEC group, twenty anesthetized and artificially ventilated rats received 1g/kg glycine (20%, iv). Five minutes later, the rats were treated with 2 mg/kg lipopolysaccharide (LPS). In control group (NS+NEC), twenty rats were treated with normal saline as a substitute for glycine. In all animals, FiO₂ was reduced after 90 min from 21% to 5% and ventilation continued until 180 min or death. At the end of the experiment, the samples of blood and intestine were obtained immediately. Serum TNFα was measured with ELISA, serum NO was determined by nitrate reductase. The histopathology of the necrotic lesions were categoried: grade Ⅰ, focal mild injury confined to villous tips; grade Ⅱ, partial loss of villi; grade Ⅲ, necrosis extending to submucosa; grade Ⅳ, transmural necrosis. RESULTS:The survival time was shorter in the NS+NEC group (P＜0.01). The intestinal injury of the rats in glycine+NEC group was markedly alleviated (P＜0.01). The levels of TNF-α and NO₂^-/NO₃^- in serum decreased significantly in animals treated with glycine (P＜0.01, P＜0.05). CONCLUSION:Glycine alleviated LPS-induced NEC by inhibiting excessive production of TNFα and nitric oxide.