虎杖苷对肺血管内皮细胞一氧化氮的影响

Effects of Polydatin on Production of Nitric Oxide in Pulmonary Endothelial Cells

目的观察虎杖苷(PD)对肺血管内皮细胞(PECs)正常及缺氧培养条件下合成一氧化氮(NO)的影响从而探讨PD抗休克的可能作用机制。方法将Griess试剂加入培养液中,用紫外分光光度计测量Griess试剂与NO2-反应的OD值,通过绘制的OD-NO2-标准曲线计算NO的值。分别观测了PD在不同时间点及不同浓度下对PECs的NO表达量的影响,并观察了PD对缺氧条件下PECs表达NO的影响。结果随着PD浓度的增加,PECs的NO表达量增高,最高为(30.86±2.83)μmol/L,与对照组相比差异有显著性(P<0.01)。随着PD作用时间的延长,PECs合成NO的量也逐渐增加,以24h最高,为(29.69±4.51)μmol/L,与起始点相比差异有显著性(P<0.01)。缺氧刺激下,PECs的NO表达量下降,PD可以对抗此作用。结论PD可能通过调节内皮细胞的NO表达量来发挥其抗休克的作用,这可能是其抗休克的分子作用机制之一。

Objective To study the anti - shock mechanism of polydatin （PD） by measuring the production of nitric oxide （NO） in pulmonary endothelial cells （PECs） stimulated by PD in normal oxygen supply and hypoxic situa- tion. Methods Concentrations of NO production, which were stimulated with PECs in different concentrations and dura- tion, were measured using ultraviolet spectrophotometer. The production of NO expression stimulated by 0.4mmoL/L PD in hypoxic PECs was also measured. Results PD significantly stimulated NO production in PECs in a concentration - de- pendent and time - dependent manners. NO production in highest PD concentration simulated PECs was significantly high- er than that in control PECs （ maximum of （30. 86± 2. 83 ） μmol/L , P 〈0. 01 ）. Meanwhile, NO expression significantly increased at 24 h comparing with baseline （ maximum of （9. 69 ±4.51 ） μmol/L, P 〈0. 01 ）. Moreover, PD reversed the NO production suppression in hypoxic PECs. Conclusion Polydafin probably up - regulates the NO production in PECs confronting shock.