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首页> 外文期刊>Cellular Physiology and Biochemistry >Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits in vitro
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Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits in vitro

机译：脂多糖诱导家兔半乳糖肠运输的抑制

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Background/Aims: Previous studies from our laboratory have revealed impaired intestinal absorption of D-galactose in lipopolysaccharide-treated rabbits. The aim of the present work was to examine the effect of LPS on D-galactose intestinal absorption in vitro. Methods: D-galactose intestinal transport was assessed employing three techniques: sugar uptake in rings of everted jejunum, transepithelial flux in Ussing-type chambers and transport assays in brush border membrane vesicles. The level of expression of the Na+/ D-galactose cotransporter (SGLT1) was analyzed by Western blot. Results: LPS decreased the mucosal D-galactose transport in rabbit jejunum but a preexposition to the endotoxin was required. LPS affected the Na+-dependent transport system by increasing the apparent Km value without affecting the Vmax. It also decreased the Na+, K+-ATPase activity. However, it did not inhibit neither the uptake of D-galactose by brush border membrane vesicles nor modified the SGLT1 protein levels in the brush border, suggesting an indirect endotoxin effect. This inhibitory effect, was reduced by selective inhibitors of Ca2+- calmodulin (W13), protein kinase C (GF 109203X), p38 mitogen-activated protein kinase (SB 203580), c-Jun N-terminal kinase (SP 600125) and mitogen extracellular kinase (U 0126). Conclusion: LPS inhibits the mucosal Na+-dependent D-galactose intestinal absorption and the Na+, K+-ATPase activity when it is added to the tissue. Intracellular processes related to protein kinases seem to be implicated in the endotoxin effect.
机译：背景/目的：我们实验室的先前研究表明，脂多糖治疗的兔的肠道D-半乳糖吸收受损。本工作的目的是研究体外脂多糖对D-半乳糖肠道吸收的影响。方法：采用三种技术评估D-半乳糖的肠运输：空肠空肠环中的糖摄取，Ussing型腔室中的上皮通量和刷状缘膜囊泡中的运输测定。通过蛋白质印迹分析Na + / D-半乳糖共转运蛋白（SGLT1）的表达水平。结果：LPS降低了兔空肠黏膜D-半乳糖的转运，但需要预先暴露于内毒素。 LPS通过增加表观Km值而不影响Vmax来影响Na +依赖性转运系统。它也降低了Na +，K + -ATPase活性。然而，它既不抑制刷状缘膜囊泡对D-半乳糖的摄取，也不改变刷状缘中的SGLT1蛋白水平，表明具有间接的内毒素作用。 Ca2 +-钙调蛋白（W13），蛋白激酶C（GF 109203X），p38丝裂原活化蛋白激酶（SB 203580），c-Jun N端激酶（SP 600125）和细胞外有丝分裂原的选择性抑制剂减弱了这种抑制作用激酶（U 0126）。结论：添加到组织中后，LPS可抑制粘膜依赖Na +的D-半乳糖肠道吸收以及Na +，K + -ATPase活性。与蛋白激酶有关的细胞内过程似乎与内毒素作用有关。

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