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口服α-干扰素可延缓非肥胖型糖尿病小鼠胰岛素依赖型糖尿病的发病。

Oral use of interferon-alpha delays the onset of insulin-dependent diabetes mellitus in nonobese diabetes mice.

作者信息

Tanaka-Kataoka M, Kunikata T, Takayama S, Iwaki K, Fujii M, Ohashi K, Ikeda M, Kurimoto M

机构信息

Fujisaki Institute, Hayashibara Biochemical Labs., Inc., Okayama, Japan.

出版信息

J Interferon Cytokine Res. 1999 Aug;19(8):877-9. doi: 10.1089/107999099313398.

DOI:10.1089/107999099313398
PMID:10476932
Abstract

Insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetes (NOD) mouse model is thought to be an autoimmune CD4 Th1-like cell-mediated disease. We tested the efficacy of oral use of interferon-alpha (IFN-alpha) therapy on IDDM in NOD mice. Using urine and blood sugar levels as indicators of IDDM, oral administration of murine IFN-alpha (100 IU/body) to NOD mice significantly delayed the onset of symptomatic diabetes. However, oral use of IFN-alpha did not prevent diabetic NOD mice from losing weight once NOD mice were symptomatic, suggesting that orally administered IFN-alpha is a prophylactic rather than therapeutic approach to the management of IDDM.

摘要

非肥胖型糖尿病(NOD)小鼠模型中的胰岛素依赖型糖尿病(IDDM)被认为是一种自身免疫性CD4 Th1样细胞介导的疾病。我们测试了口服干扰素-α(IFN-α)治疗NOD小鼠IDDM的疗效。以尿糖和血糖水平作为IDDM的指标,给NOD小鼠口服鼠源IFN-α(100 IU/只)可显著延迟症状性糖尿病的发病。然而,一旦NOD小鼠出现症状,口服IFN-α并不能阻止糖尿病NOD小鼠体重减轻,这表明口服IFN-α是一种预防而非治疗IDDM的方法。

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Low-dose oral interferon modulates expression of inflammatory and autoimmune genes in cattle.低剂量口服干扰素可调节牛体内炎症和自身免疫基因的表达。
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