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目的 观察在高脂血症动物模型形成过程中不同程度的高血脂以及DDPH对动脉血中NO、ET 1含量以及动脉壁eNOS、内皮素 1基因表达的影响。方法 在实验性家兔高脂血症模型基础上 ,采用半定量逆转录多聚酶链式反应(RT PCR)等技术 ,观察了不同时期的高脂血症对内皮素及一氧化氮代谢的影响以及DDPH的干预作用。结果 不同时期的高脂饮食可造成不同程度的高脂血症 ,相应的血管内皮细胞的内皮素 1和一氧化氮的代谢紊乱也有所不同 :轻、中度高脂血症可引起eNOS及内皮素 1mRNA表达水平升高和外周血ET 1含量增高 ;而重度高脂血症可引起eNOS及内皮素mRNA表达水平下降和外周血NOP、ET 1浓度降低 ;DDPH(ig)可明显降低实验性家兔的高血脂 ,并同时促进一氧化氮代谢产物 (NOP)、ET 1含量的升高和eNOS、ET 1mRNA的表达。结论 不同程度的高脂血症对血管内皮活性物质及其基因表达的影响是不同的。DDPH可保护血管内皮细胞 ,恢复血管活性物质合成和释放 ,从而恢复血管的反应性
Objective To observe the effects of hyperlipidemia and DDPH on the content of NO and ET 1 and the expression of eNOS and ET-1 in arterial blood in hyperlipidemia animal model. Methods Based on the experimental rabbit model of hyperlipidemia, the effects of hyperlipidemia on the metabolism of endothelin and nitric oxide were observed by semi-quantitative reverse transcriptase-polymerase chain reaction (RT PCR) DDPH intervention. Results Different periods of high-fat diet can cause different degrees of hyperlipidemia, the corresponding vascular endothelial cell endothelin 1 and nitric oxide metabolic disorders are also different: mild to moderate hyperlipidemia can cause eNOS and endothelial Elevated mRNA levels of ET-1 and ET-1 in peripheral blood increased, whereas hyperlipidemia induced a decrease of eNOS and ET-1 mRNA expression and decreased concentrations of NO and ET 1 in peripheral blood. DDPH (ig) Rabbit hyperlipemia, and at the same time promote the nitric oxide metabolites (NOP), ET 1 levels and eNOS, ET 1 mRNA expression. Conclusion Different degrees of hyperlipidemia have different effects on vascular endothelial active substances and their gene expression. DDPH protects vascular endothelial cells, restores the synthesis and release of vasoactive substances, thereby restoring vascular reactivity