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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,5min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 90min后氧吸入浓度从21％降至5％,继续机械通气至鼠死亡或存活180 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 investigate the effects of glycine on serum inflammatory cytokines IL-1 and IL-6 induced by endotoxin and hypoxia-induced necrotic enteritis (NEC) in rats. Methods 40 SD rats were randomly divided into glycine + LPS group and NS + LPS control group. In glycine group, glycine 1 g / kg was given intravenously, endotoxin 2 mg / kg was given 5 minutes later, and NS control group was treated with the same amount of saline instead of glycine. Oxygen inhalation concentration was reduced from 21% to 5% after 90min injection of LPS in all rats. Mechanical ventilation was continued until the mice died or survived for 180 min. Blood samples and small intestine samples were collected at the end of the experiment. Serum levels of IL-1 and IL-6 were measured by double-antibody sandwich ELISA. The intestinal tissues were examined for pathology and NECs were separated. Results The survival time of glycine group (159.25 ± 22.78) min was longer than that of NS control group (138.75 ± 19.05) min, the difference was significant (P <0.01). Glycine group of intestinal pathological damage was significantly lower in the control group (P <0.01). The level of serum IL-1 in glycine group was (149.1 ± 76.1) ng / L, significantly lower than that in control group (472.1 ± 505.6) ng / L (P <0.01) / L, also significantly lower than that of the control group (585.8 ± 574.5) ng / L (P <0.01). Conclusions Glycine can reduce the level of IL-1 and IL-6 in endotoxin and hypoxia-induced necrotic enteritis (NEC) rats and relieve the pathological damage of intestinal tract.