羟基红花黄色素A对心肌梗死大鼠游离脂肪酸、一氧化氮及一氧化氮合酶的影响

目的研究羟基红花黄色素A(hydroxysafflor yellow A,HSYA)对心肌梗死大鼠游离脂肪酸(FFA)、一氧化氮(NO)及一氧化氮合酶(i NOS)的影响。方法SD大鼠60只,随机分为假手术组(生理盐水1mL/100g),模型组(生理盐水1mL/100g),丹参组(40mg.kg-1),HSYA小剂量组(5mg.kg-1),HSYA中剂量组(10mg.kg-1)和HSYA大剂量组(20mg.kg-1)。除假手术组外,其余5组大鼠开胸后结扎左冠状动脉前降支建立心肌缺血模型。末次腹腔注射给药后4h腹主动脉取血,测定血清中FFA、NO含量及i NOS活性,取心脏做病理检查。结果模型组与假手术组比较,血清中FFA含量显著增高(P<0.05),HSYA小、中、大剂量组与模型组比较,血清中FFA含量无显著差异(P>0.05);模型组与假手术组比较,血清中NO含量和i NOS活性增高,但无统计学意义(P>0.05),HSYA小、中、大剂量组与模型组比较,血清中NO含量和i NOS活性均显著增高(P<0.05);病理检验显示:与模型组比较,HSYA小、中、大剂量组心肌细胞核碎裂及核溶解程度减轻,中性粒细胞浸润及纤维母细胞增生减少。结论HSYA不能降低心肌梗死后升高的FFA含量,但HSYA可明显增高i N-OS活性,催化L-精氨酸氧化生成NO,扩张冠状动脉,从而减轻结扎左冠状动脉前降支大鼠的心肌坏死程度。

Effects of hydroxysafflor yellow A on FFA,NO and iNOS in rats of myocardial infarction

OBJECTIVE To investigate the effect of Hydroxysafflor yellow A （HSYA） on FFA,NO,iNOS in rats with myocardial ischemia. METHODS Sixty SD rats were randomly devided into six groups： the sham operated group （NS 1mL/ 100g）,the model group （NS 1mL/100g）,the Danshen group （40mg·kg^-1） and the three HSYA groups：5mg·kg^-1 ,10mg·kg^-1 ,20mg·kg^-1. The model of myocardial ischemia was built up by ligating the left anterior descending branch of the coronary artery except the sham operated group. The content of FFA, NO and iNOS were measured 4h after the groups were injected the drugs via ip respectively,the pathological examination of myocardial infarction was carried out after being treated by formalin. RESULTS Compared with the sham operated group, the content of FFA in the serum improved significantly （ P 〈0. 05）,NO,iNOS also increased but had no statistical in model group （ P 〉0.05）. Compared with the model group,the content of NO,iNOS increased markedly in the HSYA treated groups （ P 〈0. 05）. Pathological examination showed：Compared with the model group, karyolysis, karyorrhexic, leukocyte infiltration and hyperplasia of fibroblast reduced in the HSYA treated groups （ P 〈0.05）. CONCLUSION HSYA could not reduce the content of FFA in rats with myocardial ischemia,but the de gree of myocardial infarction could be reduced through improving the activity of iNOS, catalyzing L--Arg producing NO to ex pand coronary artery.