摘要
目的:探讨普罗布考和辛伐他汀对高级糖基化终末产物(AGEs)诱导的大鼠肾脏微血管内皮细胞(RMECs)活性氧(ROS)含量和血红素氧合酶-1(HO-1)表达的影响。方法:体外分离和培养RMECs,将其分为对照组、AGEs损伤组、普罗布考组和辛伐他汀组;2',7'二氯荧光黄双乙酸盐(DCFH-DA)荧光染色检测各组细胞中ROS含量;逆转录聚合酶链反应法及Westernblotting检测各组细胞血红素氧合酶-1(HO-1)mRNA水平和蛋白表达。结果:(1)AGEs能上调RMECs中ROS生成和HO-1表达(P<0.05或P<0.01)。(2)普罗布考能上调RMECs中HO-1表达,能下调AGEs诱导RMECs中ROS生成和HO-1表达(P<0.05或P<0.01)。(3)辛伐他汀能下调AGEs诱导细胞ROS含量增加,但对RMECs中HO-1表达无明显影响(P>0.05)。结论:普罗布考对AGEs诱导下RMECs保护作用机制可能与其能下调内皮细胞HO-1表达有关;而同样具有抗氧化保护肾脏作用的辛伐他汀对AGEs诱导的RMECs的HO-1表达的影响不大。
AIM: To investigate the effect of probucol and simvastatin on the production of reactive oxygen species ( ROS) and heme oxygenase-1 ( HO-1) expression induced by advanced glycation end products ( AGEs) in rat renal microvascular endothelial cells ( RMECs) . METHODS: RMECs isolated and cultured from rat kidney were divided into 4 groups: normal control group,AGEs group,probucol group and simvastatin group. The levels of ROS were determined by the molecular probes of DCFH-DA. The expression of HO-1 at mRNA and protein levels was detected by RT-PCR and Western blotting,respectively. RESULTS: ( 1) AGEs up-regulated ROS production and HO-1 expression in RMECs. ( 2) Probucol up-regulated HO-1 expression in RMECs,and inhibited the increasing level of ROS and expression of HO-1 in RMECs induced by AGEs. ( 3) Simvastatin also inhibited the increasing level of ROS in RMECs induced by AGEs,but it had no effect on HO-1 expression in RMECs with or without AGEs. CONCLUSION: Protective effect of probucol on the dysfunction of RMECs induced by AGEs may be related with its effect on the expression of HO-1 at mRNA and protein levels. Simvastatin also plays roles in antioxidation and renal protection,but is ineffective in the modulation of HO-1 expression.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2010年第9期1749-1752,共4页
Chinese Journal of Pathophysiology