论文部分内容阅读
目的 探讨缺氧复氧损伤后小肠上皮细胞模型Caco 2细胞刷状缘二肽转运载体 (PepT1)生物学功能的变化及重组人生长激素(rhGH)对PepT1的调控作用。方法 建立Caco 2细胞单层培养模型和缺氧复氧损伤模型 ,比较常规培养的Caco 2细胞单层及缺氧复氧损伤后Caco 2细胞模型对底物头孢氨苄转运和摄取功能的变化 ;用rhGH对两种细胞模型进行干预 ,比较两者对底物的转运和摄取能力改变 ;同时分别比较各种情况下PepT1mRNA的变化。结果 缺氧复氧损伤后Caco 2细胞PepT1mRNA水平明显下降 ,对底物的摄取能力明显低于对照组 (P <0 0 5 ) ;正常培养的Caco 2细胞经rhGH孵育后对底物的转运和摄取能力明显强于对照组 (P <0 0 5 ) ;缺氧复氧损伤后的Caco 2细胞用rhGH孵育后对底物的转运和摄取能力明显提高 ,与单纯损伤组比较差异有统计学意义 (P <0 0 5 )。结论 缺氧复氧损伤后PepT1mRNA下降 ,在基因水平下调了肠上皮细胞刷状缘PepT1对二肽的转运和摄取能力 ;rhGH对正常培养的Caco 2细胞和缺氧复氧损伤的Caco 2细胞的二肽载体转运和摄取功能均有上调作用 ;rhGH是在基因水平调节PepT1的生物学功能
Objective To investigate the changes of biological function of brush border-associated dipeptide transporter (PepT1) in intestinal epithelial cells and the regulation of PepT1 by recombinant human growth hormone (rhGH) after hypoxia-reoxygenation injury. Methods Caco 2 cell monolayer culture model and hypoxia-reoxygenation injury model were established. Caco 2 cell monolayer culture and Caco 2 cell model were used to compare the change of substrate cephalexin transport and uptake function. rhGH intervention on the two cell models, compared the two substrates on the transport and uptake capacity changes; at the same time were compared PepT1mRNA changes in various situations. Results The level of PepT1 mRNA in Caco 2 cells decreased significantly after hypoxia-reoxygenation injury, and the substrate uptake capacity was significantly lower than that in control group (P <0.05). Caco 2 cells cultured in rhGH (P <0.05). Caco 2 cells after hypoxia-reoxygenation injury significantly increased the ability of substrate transport and uptake after incubation with rhGH, and the difference was statistically significant compared with the simple injury group (P <0 05). CONCLUSIONS: PepT1 mRNA is down-regulated after hypoxia-reoxygenation injury and down-regulated the translocation and uptake of dipeptide by PepT1 at the brush border of intestinal epithelial cells. The effect of rhGH on Caco 2 cells and hypoxia-reoxygenation-damaged Caco 2 cells Dipeptide vector transport and uptake have upregulation; rhGH is at the gene level to regulate the biological function of PepT1