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为探讨生长素调节血管钙化的可能机制 ,用肌肉注射维生素D3和口服尼古丁诱导大鼠血管钙化模型和 β 甘油磷酸盐诱导血管平滑肌细胞钙化模型 ,采用原子吸收分光光度法测定血管和细胞钙含量 ,磷酸苯二钠法测定碱性磷酸酶活性 ,4 5CaCl2 摄入测定钙沉积 ,逆转录—聚合酶链反应测定生长素、骨桥蛋白和内皮素mRNA表达水平 ,放射免疫分析方法测定血浆生长素和内皮素含量。结果表明 ,维生素D3和尼古丁明显诱导大鼠血管钙化 ,β 磷酸甘油可诱导血管平滑肌细胞钙化。采用 30和 30 0nmol kg生长素治疗大鼠均可抑制血管钙化 ,且高剂量时效应强于低剂量 ,与钙化组相比较 ,血管组织钙化指标均下降并且差异有显著性 ,而骨桥蛋白mRNA的表达明显上调。 10 - 8～ 10 - 6 mol L生长素呈浓度依赖性降低血管平滑肌细胞钙化指标 ,并上调骨桥蛋白mRNA表达。此外生长素明显下调血浆内皮素浓度及血管组织的内皮素表达 ,且高剂量生长素的效应更强。结果提示 ,生长素可能部分通过拮抗血浆和血管组织局部的内皮素系统效应而产生抑制血管组织和血管平滑肌细胞钙化的作用。
To explore the possible mechanism of auxin in regulating vascular calcification, vascular calcification model induced by intramuscular injection of vitamin D3 and oral nicotine and β-glycerophosphate-induced vascular smooth muscle cell calcification were used to determine the content of calcium in blood vessels and cells by atomic absorption spectrophotometry, Alkaline phosphatase activity was determined by phenyl-disodium phosphate method, calcium deposition was determined by 4 5 CaCl2 uptake, mRNA expression of auxin, osteopontin and endothelin were determined by reverse transcription-polymerase chain reaction (RIA), radioimmunoassay Endothelin content. The results showed that vitamin D3 and nicotine significantly induced vascular calcification in rats, and β-phosphoglycerate induced vascular smooth muscle cell calcification. The treatment with 30 and 30 nmol of auxin could inhibit the vascular calcification, and the effect of high dose was stronger than that of low dose. Compared with the calcification group, the calcification of vascular tissue decreased and the difference was significant, while osteopontin mRNA The expression was significantly increased. 10 - 8 ~ 10 - 6 mol L auxin could decrease the calcification of vascular smooth muscle cells in a concentration - dependent manner and up - regulate osteopontin mRNA expression. In addition, auxin significantly down-regulated plasma endothelin concentration and vascular endothelin expression, and the effect of high-dose auxin was stronger. The results suggest that auxin may play an inhibitory role in inhibiting the calcification of vascular tissue and vascular smooth muscle cells by antagonizing the local endothelin system effect in plasma and vascular tissue.