Rojas A, Caveda L, Romay C, López E, Valdés S, Padrón J, Glaría L, Martínez O, Delgado R
Pharmacology and Toxicology Department, Center of Pharmaceutical Chemistry, Havana, Cuba.
Biochem Biophys Res Commun. 1996 Aug 14;225(2):358-62. doi: 10.1006/bbrc.1996.1180.
We studied the role of advanced glycosylation end products on the induction of nitric oxide synthase in peritoneal mouse macrophages previously exposed to modified BSA. A dose-dependent increment in the nitric oxide production induced by LPS and IFN-gamma was observed when cell cultures were pretreated with modified BSA for 48 hours. In addition, the up regulation of nitric oxide production was also time-dependent, being maximal at 24-48 hours. Experiments carried out in the presence of neutralizing antibodies to IL-1 and TNF-alpha, suggested that up regulation was not due to the capacity of modified BSA to induce both proinflammatory signals. The up regulation of nitric oxide production was paralleled with an increase in iNOS mRNA.
我们研究了晚期糖基化终产物在诱导预先暴露于修饰牛血清白蛋白（BSA）的小鼠腹腔巨噬细胞中一氧化氮合酶方面的作用。当细胞培养物用修饰的BSA预处理48小时时，观察到脂多糖（LPS）和干扰素-γ（IFN-γ）诱导的一氧化氮产生呈剂量依赖性增加。此外，一氧化氮产生的上调也是时间依赖性的，在24 - 48小时达到最大值。在存在针对白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNF-α）的中和抗体的情况下进行的实验表明，上调并非由于修饰的BSA诱导两种促炎信号的能力。一氧化氮产生的上调与诱导型一氧化氮合酶（iNOS）mRNA的增加平行。
