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目的:探讨辛伐他汀对氧化低密度脂蛋白(ox-LDL)诱导的NRK52E细胞转分化的作用及其机制。方法:体外培养NRK-52E,同步化后分为3组:①空白对照组(NRK52E细胞+0μg·ml~(-1)ox-LDL)②ox-LDL组(NRK52E细胞+50μg·ml~(-1)ox-LDL)③辛伐他汀组(10μmol·L~(-1)辛伐他汀+50μg·ml~(-1)ox-LDL),用Western blotting测定Oxidized Low Density LiporoteinReceptor-1(LOX-1)、E-cadherin和α-SMA蛋白表达,激光共聚焦检测ROS的表达。结果:①与正常组相比,50μg·ml~(-1)ox-LDL可明显促进NRK-52E细胞LOX-1表达增高,ROS生成增多,分别为对照组的12.13倍(P<0.05)和4.83倍(P<0.05)。②随着LOX-1和ROS的增多,α-SMA表达也增多,而E-cadherin的表达则下降,分别为对照组的5.6倍(P<0.05)和0.35倍(P<0.05),NRK-52E细胞发生转分化。③10 mol·L~(-1)辛伐他汀治疗可明显抑制LOX-1表达,减少ROS生成,与50μg·ml~(-1)ox-LDL组相比,分别下降61%(P<0.05)和60%(P<0.05),随之α-SMA和E-cadherin的变化也得到部分逆转,α-SMA蛋白下降68%(P<0.05),E-cadherin蛋白上升1.82倍(P<0.05),三组比较差异均有统计学意义。结论:辛伐他汀可通过下调LOX-1表达和ROS生成,抑制ox-LDL诱导的NRK52E细胞转分化从而保护肾脏。
Objective: To investigate the effect of simvastatin on ox-LDL-induced transdifferentiation of NRK52E cells and its mechanism. Methods: NRK-52E cells were cultured in vitro and divided into three groups after synchronization. ①NRK52E cells + 0 μg · ml -1 ox-LDL ②ox-LDL group (NRK52E cells + 50μg · ml ~ (- 1) ox-LDL) ③ Simvastatin group (10μmol·L -1 simvastatin + 50μg · ml -1 ox-LDL). The expression of Oxidized Low Density Lipoprotein Receptor-1 (LOX- 1), E-cadherin and α-SMA protein expression were detected by laser confocal laser scanning microscope. Results: ①50μg · ml -1 ox-LDL significantly increased LOX-1 expression and ROS production in NRK-52E cells, which were 12.13-fold (P <0.05) and 4.83 times (P <0.05). ② With the increase of LOX-1 and ROS, the expression of α-SMA increased, while the expression of E-cadherin decreased 5.6 times (P <0.05) and 0.35 times (P < 52E cells undergo transdifferentiation. ③ Compared with 50 μg · ml -1 ox-LDL group, simvastatin treatment of 10 mol·L -1 could significantly reduce the expression of LOX-1 and decrease the production of ROS, respectively (P <0.05) And 60% (P <0.05). The changes of α-SMA and E-cadherin also partially reversed. The α-SMA protein decreased by 68% and the E-cadherin protein increased by 1.82 times (P < , The difference between the three groups was statistically significant. Conclusion: Simvastatin can protect the kidneys by down-regulating LOX-1 expression and ROS production, and inhibiting ox-LDL-induced transdifferentiation of NRK52E cells.