激动网织红核因子相关因子2对大鼠氧化应激所致血管平滑肌细胞损伤的影响

Effects of activation of nuclear factor-erythroid 2-related factor 2 on oxidative stress-induced injury of vascular smooth muscle cells in rat

目的探讨激动网织红核因子相关因子2（Nrf2）对氧化应激诱导的大鼠血管平滑肌细胞（VSMCs）损伤的影响。方法原代培养大鼠VSMCs，随机分为4组：对照组、氧化损伤组、Nrf2激动剂组、Nrf2干扰慢病毒组。Western免疫印迹法检NtJNrf2蛋白表达变化，MTT法检测各组细胞活力，Hoechst33342法及AnnexinV／FITC法检测各组细胞凋亡情况。结果荧光显微镜显示，Nrf2干扰慢病毒成功感染VSMCs；Western免疫印迹检测显示，Nrf2干扰慢病毒感染细胞后，Nrf2蛋白表达与对照组比较显著降低（P〈0．05）。与氧化损伤组比较，Nrf2激动剂组VSMCs活力显著增加（P〈0．05），细胞凋亡显著降低（P〈0．05）；而Nrf2干扰慢病毒组VSMCs活力显著减弱（P〈0．05），细胞凋亡明显增加（P〈0．05）。结论激动Nrf2能减轻氧化应激引起的VSMCs损伤，这可为VSMCs损伤的防治提出新的研究方向。

Objective To investigate the effect of the activation of nuclear factor-erythroid 2-related factor 2 （Nrf2） on the injury of rat vascular smooth muscle ceils （VSMCs） induced by oxidative stress. Methods Rat aortic VSMCs were cultured and divided into control group, oxidative damage group, Nrf2 activation group and Nrf2 siRNA-expressing lentiviral vector （Nrf2 siRNA） group. Protein level of Nrf2 was determined by Western blotting. Cell viability was measured by MTT assay, and cell apoptosis was determined by Hoechst 33342 and Annexin V/FITC. Results VSMCs were transiently transfected with Nrf2 siRNA. Nrf2 siRNA significantly inhibited the expression of Nrf2 at protein level compared to the control（P 〈 0.05）. Compared to oxidative damage group, cell viability was significantly increased （P 〈 0.05） and cell apoptosis was decreased in Nrf2 activation group（P 〈 0.05）. However, compared to oxidative damage group, cell viability was significantly decreased （P 〈 0.05） and cell apoptosis was increased in Nrf2 siRNA group（P 〈 0.05）. Conclusion Nrf2 activation can reduce oxidative stress-induced damage inVSMCs.