白细胞介素-10对血管一氧化氮/一氧化氮合酶系统的影响

Influence of interleukin-10 on nitric oxide/nitric oxide synthase system of the aorta

为探讨抗炎因子白细胞介素 10 (IL 10 )对大鼠主动脉一氧化氮 (NO) /一氧化氮合酶 (NOS)系统的影响 ,应用Griess试剂、3 H 瓜氨酸生成及蛋白免疫印迹杂交等方法 ,测定IL 10孵育对血管NO释放、NOS活性及表达的影响。结果发现细菌脂多糖 (LPS)呈浓度依赖性地激活诱导型NOS (iNOS) ,促进NO生成。IL 10 (10 -10 ～10 -8g/ml)呈浓度依赖性地上调内皮型NOS (eNOS)蛋白表达及其活性 ,但对iNOS活性及表达无明显影响。IL 10(10 -9～ 10 -8g/ml)显著抑制 10 μg/mlLPS诱导的NO生成和iNOS激活 ;而高浓度IL 10 (10 -7g/ml)则上调iNOS的活性 ,对eNOS蛋白的表达和活性无明显影响。因此IL 10对NO/NOS系统具有双重影响 ,一方面可抑制炎症介质诱发的作为炎性物质的iNOS的表达及激活 ,另一方面可上调内皮源扩血管物质NO的释放。

To study the influence of the inflammatory factorinterleukin-10 on nitric oxide (NO) and nitric oxide synthase system of rat aorta, Griess assay, production of ~ 3H-citrulline and Western blot were used to determine the release of NO, and the activity and expression of nitric oxide synthase, respectively. The results showed that lipopolysaccharide (LPS) stimulated the activity of inducible nitric oxide synthase (iNOS) and the release of NO. 10 -10 ～10 -8 g/ml of IL-10 induced the activity and expression of endothelial nitric oxide synthase (eNOS), but not of iNOS. 10 -9 ～10 -8 g/ml of IL-10 also downloaded the release of NO, and the activity and expression of iNOS induced by LPS, while 10 -7 g/ml of IL-10 significantly stimulated the activity and expression of iNOS but not eNOS. In summary, IL-10 presents a duple role in NO/NOS system. On the one hand, IL-10 inhibits the activity and expression of iNOS induced by inflammatory factor; on the other hand, IL-10 stimulates the release of endothelial NO.