胃癌患者营养状况与小肠二肽转运载体1蛋白表达的相关性

Correlation between nutritional status and expression of intestinal dipeptide transporter 1 protein in gastric cancer patients

目的研究不同营养状态胃癌患者的小肠二肽转运载体1（PEPT1）蛋白表达，探讨其可能的调控机制。方法以60例胃癌患者为研究对象，根据营养风险筛查2002（NRS2002）评分分为有营养风险组（NRS2002评分≥3分，n=18）及无营养风险组（NRS2002评分〈3分，n=42）。术中取小肠黏膜标本，Western blot法检测小肠PEPT1蛋白表达。酶联免疫吸附法检测两组胃癌患者血清肿瘤坏死因子（TNF）-α的浓度。对Caco-2细胞采用不同浓度TNF—α（20、50、100μg／L）处理，于不同时点（24、48、72h）采用Western blot法检测Caco-2细胞PEPT1蛋白表达水平。结果有营养风险组小肠PEPTI表达和血清TNF-α浓度均显著高于无营养风险组（0．63比0．23，P=0．000；0．23μg／L比0．17μg／L，P=0．001）。在Caco-2细胞模型中，不同浓度TNF—α（20、50、100μg／L）处理24h后的PEPT1表达显著高于空白组（0．68比0．54，P=0．005；0．72比0．54，P=0．001；0．78比0．54，P=0．000）；TNF-α50μg／L处理不同时间（24、48、72h）的Caeo-2细胞PEPTl表达显著高于空白组（0．57比0．52，P=0．004；0．75比0．52，P=0．000；0．77比0．52，P=0．000）。结论有营养风险的胃癌患者小肠PEPT1蛋白表达增加，其机制可能与TNF—α调控作用有关。

Objective To study the expression of intestinal dipeptide transporter 1 （ PEPTI ） protein in gastric cancer patients at different nutritional status, and to explore the possible regulatory mechanism. Methods According to Nutritional Risk Screening 2002 （ NRS 2002） score, a total of 60 gastric cancer patients were divided into nutritional risk group （ NRS 2002 score ≥ 3, n = 18） and non-nutritional risk group （ NRS 2002 score 〈 3, n = 42）. With specimens of the small intestinal mucosa taken during operation, the expression of intestinal PEPT1 protein was detected using Western blot. The serum concentration of tumor necrosis factor （TNF-ct） were measured using enzyme-linked immunosorbent assay. The expression of PEPT1 in Caco-2 cells treated with different concentrations of TNF-α （20, 50, 100 μg/L） were detected using Western blot at different time points （24, 48, 72 hours）. Results The expression of intestinal PEPT1 （0. 63 vs. 0. 23, P =0. 000） and serum TNF-α concentration （0.23 μg/L vs. 0. 17 μg/L, P =0. 001 ） in the nutritional risk group were significantly higher than those in the non-nutritional risk group. In Caco-2 cells, those treated with different concentrations of TNF-α （20, 50, 100 μg/L） for 24 hours had significantly higher PEPT1 expression than the blank group did （0.68 vs. 0. 54, P =0. 005 ; 0.72 vs. 0. 54, P =0. 001 ; 0. 78 vs. 0. 54, P =0. 000）. The Caeo-2 cells treated with 50 μg/L TNF-α for 24, 48, and 72 hours had significantly higher PEPT1 expression compared with the cells in the blank group （ 0.57 vs. 0. 52, P = 0.004; 0.75 vs. 0.52, P=0.000; 0.77 vs. 0.52, P=0.000）. Conclusion The expression of intestinal PEPT1 protein was increased in gastric eaneer patients with nutritional risk, whieh was probably attributed to the regulation of TNF-α.