Hiromatsu Y, Sato M, Tanaka K, Ishisaka N, Kamachi J, Nonaka K
Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan.
Immunology. 1993 Oct;80(2):330-2.
We investigated the effects of nicotinamide and 3-aminobenzamide (3-AB), inhibitors of poly (ADP ribose) synthetase, on phytohaemagglutinin (PHA)- or interferon-gamma (IFN-gamma)-induced intercellular adhesion molecule-1 (ICAM-1) expression on cultured thyroid cells from patients with Graves' disease. Primary cultured thyroid cells were incubated for 3 days with IFN-gamma (10-800 U/ml) or PHA (1-50 micrograms/ml) in the presence of nicotinamide, 3-AB, superoxide dismutase or catalase. The surface expression of ICAM-1 was measured by flow cytometry. Nicotinamide and 3-AB dose-dependently inhibited the induction of ICAM-1 expression by IFN-gamma or PHA on thyroid cells. Neither catalase nor superoxide dismutase, which are free-radical scavengers, inhibited the expression of ICAM-1 on thyroid cells. Our data suggest that the mechanism of the suppression of ICAM-1 expression on thyroid cells by nicotinamide is not likely to be due to the free radical scavenging. Further studies are indicated to elucidate whether the inhibition of ICAM-1 by these drugs may result in the suppression of autoimmune reaction in the thyroid gland.
我们研究了聚(ADP核糖)合成酶抑制剂烟酰胺和3-氨基苯甲酰胺(3-AB)对来自格雷夫斯病患者的培养甲状腺细胞上植物血凝素(PHA)或干扰素-γ(IFN-γ)诱导的细胞间黏附分子-1(ICAM-1)表达的影响。将原代培养的甲状腺细胞在烟酰胺、3-AB、超氧化物歧化酶或过氧化氢酶存在的情况下,用IFN-γ(10 - 800 U/ml)或PHA(1 - 50微克/毫升)孵育3天。通过流式细胞术测量ICAM-1的表面表达。烟酰胺和3-AB剂量依赖性地抑制IFN-γ或PHA对甲状腺细胞ICAM-1表达的诱导。自由基清除剂过氧化氢酶和超氧化物歧化酶均未抑制甲状腺细胞上ICAM-1的表达。我们的数据表明,烟酰胺抑制甲状腺细胞上ICAM-1表达的机制不太可能是由于自由基清除。需要进一步研究以阐明这些药物对ICAM-1的抑制是否可能导致甲状腺自身免疫反应的抑制。