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

无法合成抗坏血酸的ODS大鼠抗坏血酸缺乏引起的炎症样反应分析。

• 批准号: 13660121
• 负责人: HORIO Fumihiko
• 金额: $ 2.3万
• 依托单位: Nagoya University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13660121/
• 关键词: Ascorbic acid; ODS rat; Ascorbic acid deficiency; Acute phase protein; Inflammation; Interleukin-6; Chemokine; Cytokine; ビタミンC

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.

作为抗坏血酸（维生素C）的一种新功能，我们发现，抗坏血酸缺乏导致ODS大鼠肝脏急性时相蛋白基因表达的刺激，不能合成抗坏血酸。抗坏血酸缺乏的ODS大鼠血清中炎性细胞因子IL-6和炎性趋化因子CINC-1的浓度升高，但无生长迟缓。抗坏血酸缺乏型ODS大鼠肝脏CINC-1 mRNA水平高于对照型ODS大鼠。在这项研究中，我们假设，抗坏血酸缺乏引起的interleikin-6和CINC-1的基因表达的刺激，在肝脏由于内毒素从肠腔流入门静脉。然而，我们没有观察到与我们假设相反的结果，我们也在维持一种新的自发性高血压大鼠品系的殖民地，该品系不能合成抗坏血酸，SHR-od。高血压与氧化应激密切相关已成为研究热点。在本研究中，我们发现，血清和组织中的抗坏血酸浓度SHR-od显着低于正常血压ODS大鼠。这些低浓度可能是由加速SHR-od中的抗坏血酸降解相比，ODS大鼠。这一结果表明，高血压患者对抗坏血酸的需求增加。

项目成果

Ohno, T.: "Blood and liver concentrations in EDS Shrews exhibiting spontaneous non-insulin dependent diabetes mellitus (NIDDM)"Exp. Anim.. 50(5). 427-429 (2001)

Ohno, T.：“表现出自发性非胰岛素依赖型糖尿病 (NIDDM) 的 EDS 鼩鼱的血液和肝脏浓度”Exp。

Tsuda, T.: "Cyanidin 3-O-β-D-glucoside suppreses nitric oxide production during a zymosan treatment in rats"J. Nutr. Sci. Vitaminol.. 48(4). 305-310 (2002)

Tsuda, T.：“花青素 3-O-β-D-葡萄糖苷在大鼠酵母聚糖治疗过程中抑制一氧化氮的产生”J. Nutr Sci. 48(4) (2002)。

Minakata,K., Suzuki,O., Saito,S., Kawai,K. and Horio,F.: "Effects of paraquat on essential antioxidant elements in osteogenic diorder Shionogi rat"J.Toxicol.Environ.Health. 65. 143-147 (2002)

Minakata,K.、铃木,O.、Saito,S.、Kawai,K.

Anunciado,R.V.R, Nishimura,M., Mori,M., Ishikawa,A., Tanaka,S., Horio,F., Ohno,T. and Namikawa,T.: "Quantitative trait loci for body weight in the intercross between SM/J and A/J mice"Exp.Anim.. 50. 319-324 (2001)

Anunciado，R.V.R，西村，M.，森，M.，石川，A.，田中，S.，堀尾，F.，大野，T。

Minakata,K., Kawai,K., Horio,F., Nozawa,H., Watanabe-Suzuki,K. and Suzuki,O.: "Diquat markedly changes iron and copper concentrations in tissues and plasma of ODS rats"Jpn.J.Forensic Toxicol.. 20. 277-283 (2002)

Minakata,K.、Kawai,K.、Horio,F.、Nozawa,H.、Watanabe-Suzuki,K.