西红花酸对动脉粥样硬化鹌鹑血清一氧化氮含量的影响及其机制

目的：观察西红花酸（CCT）对动脉粥样硬化（AS）鹌鹑血清一氧化氮（NO）含量的影响并探讨其可能的作用机制.方法：用高脂饲料复制鹌鹑AS模型并灌胃给予CCT,9周后做主动脉HE染色观察AS病理变化、酶法测定血清中NO含量;培养牛主动脉内皮细胞（BAECs）,用氧化低密度脂蛋白（OX-LDL）作用后测定培养液中NO含量和细胞中内皮源性NOS（eNOS）、诱导型NOS（iNOS）活性,RT-PCR方法测定eNOS基因表达水平,观察CCT对上述指标的影响.结果：CCT（25,50,100 mg/kg）能够明显改善鹌鹑AS病变,显著升高AS鹌鹑血清中NO含量;OX-LDL能显著减少BAECs培养液中NO含量,降低细胞内eNOS活性,下调eNOS mRNA表达水平.CCT（1,10 μmol/L）能显著增加OX-LDL作用后细胞培养液中NO含量,提高细胞内eNOS活性、上调eNOS mRNA表达水平.OX-LDL和CCT对细胞内iNOS活性没有明显影响.结论：CCT能显著增加AS鹌鹑血清NO含量,提高OX-LDL作用后牛主动脉内皮细胞NO含量和eNOS活性,其机制与CCT上调eNOS mRNA表达水平有关.

Effects of Crocetin on Serum Nitric Oxide Content of Atherosclerotic Quail and Its Mechanism

AIM: The purpose of this study was to investigate the effect of crocetin (CCT) on serum nitric oxide (NO) content of atherosclerotic (AS) quail and to explore its underlying mechanisms. METHOD: AS quail model was established by feeding high lipid food to quail and CCT was administered by oral gavage. 9 weeks later the pathological changes of aorta arch was observed and serum NO content was determined. Bovine aortic endothelial cells (BAECs) pretreated with different means were cultured with OX-LDL for 24 h. Nitric oxide (NO) content in culture medium and activities of both endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) in cells were examined using commercially available kits. The mRNA expression of eNOS was measured by RT-PCR assay. RESULT:CCT(25,50,100 mg/kg)could significantly alleviate the pathological changes of aorta arch and inhibit the reduction of serum NO content of AS quail. OX-LDL was found to reduce both activity and mRNA expression of eNOS in BAECs and subsequently decrease the NO content in culture medium of cells. Pretreatment with CCT (1, 10 μmol/L)remarkably inhibited the reduction of both activity and mRNA expression of eNOS in BAECs and correspondingly increased NO content. Both OX-LDL and CCT had no effect on iNOS activity. CONCLUSION: CCT could significantly inhibit the reduction of serum NO content of AS quail and that of BAECs pretreated with OX-LDL, which was partly due to the upregulation of eNOS mRNA expression.