目的: 研究木兰脂素(magnolin,Mag)的舒张血管作用、作用机制和细胞毒性。 方法: 应用离体血管环技术观察Mag对大鼠胸主动脉环张力的作用,记录去氧肾上腺素 (phenylephrine,PE,1 μmolL-1)预收缩的离体大鼠胸主动脉环张力变化。采用一氧化氮合酶(eNOS) 抑制剂L-硝基精氨酸甲酯(L-NAME,100 μmolL-1)预处理后观察Mag对血管环张力改变的 影响,并用MTT方法观察对大鼠肾细胞(NRK)增殖的影响。 结果: 木兰脂素(0.1~1 000 μmolL-1)对PE预收缩的血管环具有浓度依赖的舒张作用,该舒张作用为内皮依赖性。50%最大效应浓度(Half maximal effective concentration,EC50)为24.43 μmolL-1。 内皮型一氧化氮合酶(endothelial nitric oxide synthesis,eNOS)抑制剂-NG-硝基-L-精氨酸甲酯(NG-Nitro-L-arginine methyl ester hydrochloride,L-NAME,100 μmolL-1)预处理可以抑制Mag对具内皮血管的舒张效应。木兰脂素(0.1~1 000 μmolL-1)处理NRK的相对增殖率在84.17%和134.60%。 结论: 木兰脂素具有内皮依赖性舒张血管作用,其机制可能与内皮型一氧化氮合成酶激活有关,且没有肾细胞毒性。
Objective: To characterize vasodilatative effect of magnolin (Mag) on isolated rat thoracic aorta,elucidate its possible action mechanism,and its toxicity in rat renal cells NRK in vitro. Method: The thoracic aorta was isolated from male Sprague-Dawley (SD) rats and the isometric tension of aortic rings induced by phenylephrine (PE,1 μmol L-1) were measured. To investigate the vasodilation effect of Mag on it were observed in the rings with endothelium intact or endothelium denuded. The rat renal cells NRK were cultured in vitro and MTT assay. Result: Mag (0.1-1 000 μmol L-1) produced concentration-dependent response,relaxations in PE-contracted aortic rings with endothelium. The half maximal effective concentration (EC50) of Mag was 24.43 μmol L-1. The vasodilatative effect by Mag was not statistically inhibited by 100 μmol L-1 (L-NAME) in the preparations with endothelium. The relative growth rates (RGR) of Mag (0.1-1 000 μmol L-1) were between 84.17% and 134.60%. Conclusion: Magnolin causes relaxation of aortic ring through endothelium-dependent pathway. The mechanisms might be involved in eNOS. Magnolin is safe to rat renal cells NRK with concentration between 0.1 μmol L-1and 1 000 μmol L-1.