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目的探讨替米沙坦对人血管内皮细胞血管紧张素转换酶2(ACE2)表达的影响。方法原代培养人脐静脉内皮细胞(HUVECs),以替米沙坦(终浓度分别为10-7、10-6、10-5mol/L)刺激24h;以替米沙坦(终浓度为10-6mol/L)分别刺激6、12和24h;以2型血管紧张素受体特异性阻断剂PD123319(终浓度为10-6mol/L)单独或与相同终浓度的替米沙坦联合刺激12h。以蛋白质免疫印迹法(Westernblot)检测ACE2蛋白表达量,以逆转录聚合酶链反应(RTPCR)检测ACE2mRNA表达。结果替米沙坦呈剂量(浓度)和时间依赖性使ACE2蛋白及基因表达量显著增加。与对照组比较,替米沙坦在终浓度分别为10-7、10-6、10-5mol/L时,可使ACE2蛋白表达量分别增加1.5、2.7和4.6倍,使ACE2mRNA表达分别增加1.2、2.3和4.5倍;于6、12和24h,替米沙坦(终浓度10-6mol/L)分别使ACE2蛋白表达量增加1.6、2.7和4.2倍,使ACE2mRNA表达分别增加1.3、2.3和4.0倍;与对照组及替米沙坦组比较,PD123319对ACE2蛋白及基因表达无影响。结论替米沙坦呈剂量(浓度)和时间依赖性显著上调ACE2蛋白及基因表达,此作用可能与阻断血管紧张素受体无关。
Objective To investigate the effect of telmisartan on the expression of angiotensin-converting enzyme 2 (ACE2) in human vascular endothelial cells. Methods Primary cultured human umbilical vein endothelial cells (HUVECs) were treated with telmisartan (10-7, 10-6, and 10-5 mol / L, respectively) for 24 h. Telmisartan -6 mol / L) for 6, 12 and 24 h, respectively. Combined with type 2 angiotensin receptor-specific blocker PD123319 (final concentration 10-6 mol / L) alone or in combination with telmisartan 12h. The expression of ACE2 protein was detected by Western blotting and ACE2 mRNA expression was detected by reverse transcriptase polymerase chain reaction (RTPCR). Results Telmisartan significantly increased ACE2 protein and gene expression in a dose-and time-dependent manner. Compared with the control group, telmisartan increased ACE2 protein expression by 1.5, 2.7 and 4.6 times when the final concentrations were 10-7, 10-6 and 10-5 mol / L, respectively, and increased ACE2 mRNA expression by 1.2 , 2.3 and 4.5 times; at 6, 12 and 24h, telmisartan (final concentration 10-6mol / L) increased ACE2 protein expression by 1.6, 2.7 and 4.2 times, respectively, ACE2mRNA expression increased by 1.3, 2.3 and 4.0 Fold; compared with control group and telmisartan group, PD123319 had no effect on ACE2 protein and gene expression. Conclusion Telmisartan significantly up-regulated ACE2 protein and gene expression in a dose-and time-dependent manner, which may not be related to angiotensin receptor blockade.