益肺活血复方对人肺动脉内皮细胞分泌功能的影响

目的研究益肺活血复方对人肺动脉内皮细胞分泌功能的影响。方法建立人肺动脉内皮细胞低氧高二氧化碳模型;制备益肺活血复方不同给药剂量（生药10、20、40 g.kg-1）的含药血清及生理氯化钠溶液血清;在细胞培养液中共同孵育12 h后,利用免疫组织化学法测定细胞内低氧诱导因子-1ɑ（HIF-1ɑ）的表达,放射免疫分析法测定各组细胞上清液中内皮素-1（ET-1）的浓度,逆转录多聚酶链反应法测定ET-1mRNA的表达水平。结果低氧高二氧化碳条件下,人肺动脉内皮细胞ET-1的分泌、HIF-1ɑ蛋白和ET-1mRNA的表达明显增强（P〈0.05）;而中、高浓度益肺活血复方能够抑制人肺动脉内皮细胞合成分泌HIF-1ɑ、ET-1mRNA及ET-1（P〈0.05）。结论低氧高二氧化碳导致人肺动脉内皮细胞功能障碍,而中、高浓度的益肺活血复方可减少人肺动脉内皮细胞ET-1的分泌和ET-1mRNA、HIF-1α蛋白的表达,从而减轻人肺动脉内皮细胞功能紊乱的程度,益肺活血复方可能成为治疗低氧高二氧化碳性肺动脉高压的有效药物。

Effect of Compound Yifei Huoxue on Secretion Function of Human Pulmonary Arterial Endothelial Cells

Objective To investigate the effect of Compound Yifei Huoxue （CYH） on secretion function of human pulmonary arterial endothelial cells. Methods A model of hypoxia hypercapnia was established. Using meth- ods of pharmacology, we added different doses of pharmacy （crude drug 10,20,40 g ·kg -1 ） into the culture medi- um to produce serum containing CYH and serum containing 0.9% NaCl. After co-incubation for 12 h, the expres- sion lbvel of HIF-1 u was tested with immunohistochemistry method, ET-1 level with radioimmunoassay, and ET-1 mRNA level with RT-PCR. Results Hypoxia hypercapnia significantly increased secretion of ET-1 （ P 〈 0.01 ）, expression of HIF-1 a protein （ P 〈 0.01 ） and ET-1 mRNA （ P 〈 0.05 ）, while CYH （ moderate, high concentra- tion） inhibited the expression of ET-1 （ P 〈 0.01 ）, HIF-1α （ P 〈 0.05） and ET-1 mRNA （ P 〈 0.05 ）. Conclu- sion Hypoxia, hypercapnia causes pulmonary vascular endothelial dysfunction. CYH（ moderate, high concentration） can directly decrease ET-1 levels and the expression of HIF-1α and ET-ImRNA of human pulmonary artery endo- thelial cells under hypoxia hypercapnia, thus alleviating endothelial dysfunction. CYH can possibly help prevent hypoxia hypercapnia pulmonary arterial hypertension.