The analysis of inflammation-like response caused by ascorbic acid deficiency in ODS rats unable to synthesize ascorbic acid.

作为抗坏血酸(维生素C)的一种新功能，我们发现抗坏血酸缺乏会刺激肝组织急性期蛋白基因的表达，使其不能合成抗坏血酸。血清中炎性细胞因子IL-6和炎性趋化因子CINC-1的浓度在抗坏血酸缺乏的ODS大鼠中升高，但没有生长迟缓。抗坏血酸缺乏组大鼠肝组织CINC-1mRNA水平高于对照组。在这项研究中，我们假设抗坏血酸缺乏导致内毒素从肠腔流入门静脉而刺激肝脏IL-6和CINC-1基因的表达。然而，我们无法观察到支持我们假设的结果。我们还维持了一种新的自发性高血压大鼠株系的克隆，该株不能合成抗坏血酸，SHR-OD。高血压伴发氧化应激已成为研究热点。在本研究中，我们发现SHR-OD大鼠的血清和组织中抗坏血酸浓度显著低于正常血压的ODS大鼠。这些低浓度可能是由于SHR-OD大鼠的抗坏血酸降解速度比消耗臭氧层物质大鼠加快所致。这一结果提示高血压患者对抗坏血酸的需求增加。

As a new function of ascorbic acid (vitamin C), we found that ascorbic acid deficiency caused the stimulation of hepatic expression of acute phase proteins genes in ODS rat unable to synthesize ascorbic acid. Serum concentrations of interleukin-6, an inflammatory cytokine, and CINC-1, an inflammatory chemokine, were elevated in ascorbic acid-deficient ODS rats without growth retardatioon. The hepatic CINC-1 mRNA level was higher in ascorbic acid-deficient ODS rats than that in the control ODS rats. In this study, we hypothesized that ascorbic acid deficiency caused the stimulation of interleikin-6 and CINC-1 genes expression in liver due to influx of endotoxin from the intesitinal lumen to portal vein. However, we could not observe the results supportiong our hypothesis.We are also maintaining the colony of a novel strain of spontaneously hypertensive rat unable to synthesize ascorbic acid, SHR-od. It has been focused that hypertention accompanies with oxidative stress. In this study, we found that serum and tissue concentrations of ascorbic acid in SHR-od were markedly lower than those in normotensive ODS rats. These low concentrations might be caused by the acceleration of ascorbic acid degradation in SHR-od compared to ODS rats. This result suggests that the requirement of ascorbic acid is increased in hypertensive patients.