Horio Fumihiko, Kiyama Keiichiro, Kobayashi Misato, Kawai Kaori, Tsuda Takanori
Department of Food & Nutritional Sciences, College of Bioscience and Biotechnology, Chubu University, Aichi, Japan.
J Nutr Sci Vitaminol (Tokyo). 2006 Feb;52(1):28-32. doi: 10.3177/jnsv.52.28.
ODS rat has a hereditary defect in ascorbic acid biosynthesis and is a useful animal model for elucidating the physiological role of ascorbic acid. We previously demonstrated by using ODS rats that ascorbic acid deficiency changes the hepatic gene expression of acute phase proteins, as seen in acute inflammation. In this study, we investigated the effects of ascorbic acid deficiency on the production of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 (CINC-1), in ODS rats. Male ODS rats (6 wk of age) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Obvious symptoms of scurvy were not observed in the ascorbic acid-deficient rats. Ascorbic acid deficiency significantly elevated the serum concentration of CINC-1 on d 14. The liver and spleen CINC-1 concentrations in the ascorbic acid-deficient rats were significantly elevated to 600% and 180% of the respective values in the control rats. However, the lung concentration of CINC-1 was not affected by ascorbic acid deficiency. Ascorbic acid deficiency significantly elevated the hepatic mRNA level of CINC-1 (to 480% of the value in the control rats), but not the lung mRNA level. These results demonstrate that ascorbic acid deficiency elevates the serum, liver and spleen concentrations of CINC-1 as seen in acute inflammation, and suggest that ascorbic acid deficiency stimulate the hepatic CINC-1 gene expression.
ODS大鼠在抗坏血酸生物合成方面存在遗传性缺陷，是用于阐明抗坏血酸生理作用的有用动物模型。我们之前利用ODS大鼠证明，抗坏血酸缺乏会改变急性期蛋白的肝脏基因表达，这在急性炎症中可见。在本研究中，我们调查了抗坏血酸缺乏对ODS大鼠炎症趋化因子——细胞因子诱导的中性粒细胞趋化因子-1（CINC-1）产生的影响。给雄性ODS大鼠（6周龄）喂食含抗坏血酸（300毫克/千克饲料）的基础饲料或不含抗坏血酸的饲料，持续14天。在抗坏血酸缺乏的大鼠中未观察到明显的坏血病症状。抗坏血酸缺乏在第14天时显著提高了血清CINC-1浓度。抗坏血酸缺乏大鼠的肝脏和脾脏CINC-1浓度分别显著升高至对照大鼠相应值的600%和180%。然而，肺中CINC-1浓度不受抗坏血酸缺乏的影响。抗坏血酸缺乏显著提高了肝脏中CINC-1的mRNA水平（达到对照大鼠值的480%），但未提高肺中的mRNA水平。这些结果表明，抗坏血酸缺乏会像在急性炎症中那样提高血清、肝脏和脾脏中CINC-1的浓度，并提示抗坏血酸缺乏会刺激肝脏CINC-1基因表达。
