肿瘤坏死因子对谷氨酰胺促大鼠小肠蛋白质合成的影响及途径

发布时间：2018-07-24 10:27

【摘要】：目的谷氨酰胺(glutamine,Gln)需经过载体转运至细胞内才能被利用,感染状态下Gln疗效不佳。肿瘤坏死因子(tumor necrosis factor,TNF-α)是感染中重要的调节因子,故研究TNF-α与Gln促蛋白质合成及其与Gln载体之间的关系对揭示感染状态下Gln代谢途径、提高疗效具有重要意义。文章研究TNF-α对Gln促大鼠小肠蛋白质合成及其对细胞膜Gln载体ASCT2mRNA、蛋白表达的影响,揭示TNF-α影响Gln促蛋白质合成的途径。方法 30只雄性SD大鼠按单纯随机法分3组:对照组、Gln组和TNF-α组。所有大鼠均行3 d全肠外静脉营养。对照组仅给予普通全肠外营养;Gln组给予添加丙氨酰谷氨酰胺二肽的肠外营养,Gln剂量为0.3 g/(kg·d),计72 h;TNF-α组给予添加丙氨酰谷氨酰胺二肽的肠外营养,并在第3天持续24h静脉滴注TNF-α,速度5μg/(kg·h)。所有大鼠均在取材前0.5h一次性静脉注射[L-15N]亮氨酸,剂量1.0 mmol/kg。实验结束时分别测定血浆TNF-α、Gln浓度、小肠Gln浓度、蛋白质合成率、ASCT2载体mRNA及蛋白表达水平。结果 TNF-α组血浆TNF-α浓度显著高于其他2组;TNF-α组血浆及小肠中Gln浓度最高;Gln组和TNF-α组小肠中蛋白质合成率均高于对照组,且Gln组最高;以上各组之间差异有统计学意义(P0.01)。对照组ASCT2的mRNA及蛋白表达均显著低于其他2组(P0.01)。Gln组ASCT2的蛋白显著高于其他2组(P0.01)。结论 TNF-α能够升高大鼠血浆及小肠中Gln的浓度,抑制Gln的促蛋白质合成作用,其途径是TNF-α抑制氨基酸载体的转运功能,Gln不能顺利进入细胞,导致组织蛋白质合成下降,这种抑制发生在翻译及以后水平。
[Abstract]:Objective glutamine (Gln) needs to be transported through the carrier to the cell, and the effect of Gln is not good. The tumor necrosis factor (TNF- alpha) is an important regulatory factor in the infection. Therefore, the study of the relationship between TNF- alpha and Gln promoting protein synthesis and its Gln carrier is to reveal the Gln generation in the infection state. This article studies the effect of TNF- alpha on the protein synthesis of small intestine in Gln rats and its effect on the expression of Gln carrier ASCT2mRNA and protein in the cell membrane, and reveals the way that TNF- alpha affects the synthesis of protein by Gln. Methods 30 male SD rats were divided into 3 groups according to the simple random method: the control group, the Gln group and the TNF- alpha group. All the rats were all in the control group. 3 D total parenteral nutrition was performed in the control group. The control group was given only general parenteral nutrition; group Gln was given parenteral nutrition with alamyl glutamine two peptide, Gln dose 0.3 g/ (kg. D), 72 h; TNF- a group was given parenteral nutrition with alamyl glutamine two peptide, and TNF- a continued 24h intravenous drip of TNF- alpha at third days, and all rats were 5 micron g/ (kg.). The plasma TNF- alpha, Gln concentration, Gln concentration, protein synthesis rate, ASCT2 carrier mRNA and protein expression level were measured at the end of 1 mmol/kg. experiment at the end of the 1 mmol/kg. experiment. Results the concentration of TNF- a in the TNF- alpha group was significantly higher than that of the 2 groups; TNF- Alpha Group was the highest in the plasma and small intestine. The protein synthesis rate in the small intestine of group n and TNF- alpha was higher than that in the control group, and the highest in the Gln group, and the difference between the above groups was statistically significant (P0.01). The mRNA and protein expression of ASCT2 in the control group was significantly lower than that of the other 2 groups (P0.01).Gln group ASCT2 significantly higher than the other 2 groups (P0.01). Conclusion TNF- alpha could increase the plasma and small intestine Gln in rats. The concentration of Gln inhibits the synthesis of protein and the pathway is that TNF- alpha inhibits the transport of amino acid carriers, and Gln does not enter cells successfully, causing the decrease of tissue protein synthesis, which occurs at translation and later levels.
【作者单位】：南京军区南京总医院烧伤整形科;解放军普通外科研究所;
【基金】：国家自然科学基金(30271263)
【分类号】：R363

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