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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Treatment with glutamine is associated with down-regulation of Toll-like receptor-4 and myeloid differentiation factor 88 expression and decrease in intestinal mucosal injury caused by lipopolysaccharide endotoxaemia in a rat.
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Treatment with glutamine is associated with down-regulation of Toll-like receptor-4 and myeloid differentiation factor 88 expression and decrease in intestinal mucosal injury caused by lipopolysaccharide endotoxaemia in a rat.

机译：用谷氨酰胺治疗与大鼠Toll样受体4和髓样分化因子88表达的下调以及脂多糖内毒素血症引起的肠粘膜损伤的减少有关。

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Recent evidence suggests that lipopolysaccharide (LPS) endotoxaemia in a rat causes significant mucosal injury. Our objective was to determine the effects of glutamine (Gln) on Toll-like receptor 4 (TLR-4), myeloid differentiation factor 88 (Myd88) and tumour necrosis factor (TNF)-alpha receptor-associated factor 6 (TRAF6) expression in intestinal mucosa following LPS endotoxaemia in a rat. For this purpose, male Sprague-Dawley rats were assigned randomly to one of three experimental groups of 10 rats each: (i) control rats underwent intraperitoneal (i.p.) injection of sterile saline once a day; (ii) rats were treated with LPS given i.p. once a day at a dose of 10 mg/kg for 48 h (two doses); and (iii) rats were pretreated with oral Gln given in drinking water (2%) 48 h before and following injection of LPS. Intestinal mucosal parameters, enterocyte proliferation and apoptosis were determined at death. TLR-4 and MyD88 mRNA expression was measured with reverse transcription-polymerase chain reaction (RT-PCR). TLR-4 and MyD88 protein expression were analysed by Western immunoblotting. We observed a statistically significant (P < 0.05) decrease in mucosal weight, mucosal DNA and enterocyte proliferation and a significant increase in enterocyte apoptosis in rat intestine, following LPS administration. These changes were attenuated significantly by dietary Gln. Expression of TLR-4, MyD88 and TRAF6 mRNA in the mucosal ileum was significantly higher in LPS rats versus control rats (P = 0.0006, P = 0.0015, P = 0.03, respectively) as well as TLR-4 and MyD88 protein expression. The administration of Gln reduced significantly the expression of TLR-4, MyD88 and TRAF6 (P = 0.023, P = 0.014, P = 0.035, respectively) mRNA as well as TLR-4 and MyD88 protein expression in ileum compared to LPS animals. We did not find a significant change in the expression of TLR-4, MyD88 or TRAF6 in the jejunum of different groups. We conclude that treatment with Gln was associated with down-regulation of TLR-4, MyD88 and TRAF6 expression and concomitant decrease in intestinal mucosal injury caused by LPS endotoxaemia in a rat.
机译：最近的证据表明，大鼠体内的脂多糖（LPS）内毒素血症可引起严重的粘膜损伤。我们的目的是确定谷氨酰胺（Gln）对Toll样受体4（TLR-4），髓样分化因子88（Myd88）和肿瘤坏死因子（TNF）-α受体相关因子6（TRAF6）表达的影响。大鼠LPS内毒素血症后肠粘膜为此，将雄性Sprague-Dawley大鼠随机分为三个实验组，每组10只。（i）对照组大鼠每天一次腹膜内（i.p.）注射无菌盐水; （ii）给大鼠腹膜内注射LPS治疗。每天一次，剂量为10 mg / kg，持续48小时（两次）; （iii）在注射LPS之前和之后48小时，在口服饮用水（2％）中给予口服Gln预处理大鼠。死亡时测定肠粘膜参数，肠上皮细胞增殖和凋亡。用逆转录-聚合酶链反应（RT-PCR）测量TLR-4和MyD88 mRNA的表达。通过Western免疫印迹分析TLR-4和MyD88蛋白表达。我们观察到，LPS给药后，大鼠肠道粘膜重量，粘膜DNA和肠上皮细胞增殖显着（P <0.05）降低，肠上皮细胞凋亡显着增加。这些变化被饮食中的谷氨酸显着减弱。在LPS大鼠中，粘膜回肠中TLR-4，MyD88和TRAF6 mRNA的表达明显高于对照组（分别为P = 0.0006，P = 0.0015，P = 0.03）以及TLR-4和MyD88蛋白的表达。与LPS动物相比，Gln的给药显着降低了回肠中TLR-4，MyD88和TRAF6的表达（分别为P = 0.023，P = 0.014，P = 0.035）以及TLR-4和MyD88蛋白表达。我们未发现不同组空肠中TLR-4，MyD88或TRAF6的表达有显着变化。我们得出的结论是，用Gln治疗与TLR-4，MyD88和TRAF6表达下调以及大鼠LPS内毒素血症引起的肠粘膜损伤的减少有关。

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