Pioneer study on the protective effect of ascorbic acid on barrier function of gastrointestinal tract

在遗传性抗坏血酸(维生素C)生物合成缺陷的ODS大鼠中，我们已证明抗坏血酸缺乏刺激肝脏急性时相蛋白基因的表达，这些基因在炎症中可见。我们推测，抗坏血酸缺乏引起的肠道功能紊乱导致内毒素从胃肠道流入门静脉，从而导致肝脏的炎症反应。经本研究分析，抗坏血酸缺乏组门静脉血中内毒素浓度明显高于对照组。随后，我们确认了使用抗生素治疗的抗坏血酸缺乏的消耗臭氧层物质大鼠是否出现了肝脏炎症反应。结果观察大鼠肝脏炎症反应。根据这些结果，我们推测内毒素流入门静脉和其他由抗坏血酸缺乏引起的未知疾病导致了肝脏的炎症反应。然而，本研究首次证实抗坏血酸缺乏可导致ODS大鼠胃肠道功能障碍和内毒素血症。

In ODS rats with a hereditary defect of ascorbic acid (vitamin C) biosynthesis, wehave demonstrated that ascorbic acid deficiency stimulate the hepatic expressions of acute phase protein genes, that were seen in inflammation. We hypothesized that the intestinal disorder provoked by ascorbic acid deficiency causes the inflow of endotoxin from gastrointesinal tract into portal vein, leading to the inflammatory responses in liver. By the analysis in this study, the endotoxin concentration in portal vein was significantly higher in the ascorbic acid-deficient group than that in the control group. Subsequetly, we confirmed whether the hepatic inflammatory responses occur or do not in ascorbic acid-deficient ODS rats treated with antibiotics. As a result, the hepatic inflammatory response was observed. From these results, we speculate that the inflow of endotoxin into the portal vein and the other unknown disorder by ascorbic acid deficiency cause the inflammatory responses in liver. However, this study demonstrated for the first time that ascorbic acid deficiency induce the disfunction of gastrointestinal tract and endotoxemia in ODS rats.