tBHQ通过Nrf2通路抗脂多糖诱导人脐静脉内皮细胞损伤中的作用及机制  

Effects of tBHQ on Lipoppolysacchride-Induced Impairment of Human Umbilial Vein Endothelial Cell by Nuclear Factor-Erythroid 2 p45-Related Factor 2

作　　者：曾慰[1] 肖新华[2] 胡名松[1] 邓宏军[1] 胡军[1] 郑达扬[1] 高文奎[1] 

机构地区：[1]南华大学附属第二医院胸外科,湖南省衡阳市421001 [2]南华大学附属第一医院内分泌实验室,湖南省衡阳市421001

出　　处：《中国动脉硬化杂志》2011年第7期552-556,共5页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(81070667)

摘　　要：目的探讨叔丁基对苯二酚(tBHQ)在抗脂多糖诱导人脐静脉内皮损伤中的作用及相关机制。方法体外培养人脐静脉内皮细胞,用脂多糖作用建立人脐静脉内皮损伤模型前,用不同浓度叔丁基对苯二酚预处理24h。用MTT法检测内皮细胞活性,Western blot检测细胞核内和核外转录因子NF-E2相关因子2(Nrf2)蛋白表达,DCFH-DA染色法检测细胞内活性氧量,Western blot和ELISA检测肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平。结果与对照组相比,脂多糖处理能够显著降低细胞活性,而叔丁基对苯二酚能够显著抑制脂多糖的损伤作用(P<0.05)。与脂多糖单独处理组相比,叔丁基对苯二酚预处理能够显著增加核内Nrf2蛋白水平,并显著降低活性氧、肿瘤坏死因子α、白细胞介素1β和白细胞介素6水平(P<0.05)。结论叔丁基对苯二酚能够通过诱导Nrf2的核转位来抑制脂多糖诱导的活性氧和炎症因子增加,起到抗内皮细胞损伤作用。Aim To investigate the role and mechanism of tert-butylhydroquinone （tBHQ） on lipoppolysacchride （LPS）-induced impairment of human umbilial vein endothelial cell （HUVEC）. Methods Before treated with LPS, HUVEC were cultured with tBHQ in vitro. MTT analysis measured the effects of LPS and tBHQ on HUVEC ; Western blot analysis measured the effects of tBHQ on the levels of Nrf2 in HUVEC ; DCFH-DA measured the effects of tBHQ on the levels of ROS; Western blot and ELISA analysis measured the effects of tBHQ on the levels of TNF-α, IL-1β and IL-6. Results Compared with control group, viabilities of HUVEC were decreased significantly by LPS （ P 〈 0. 05）. However, the effects of LPS could be attenuated notably by tBHQ （P 〈 0. 05）. Pretreatment with tBHQ could increase the expression of nuclear Nrf2 protein significantly （P 〈 0.-05 ）, and reduce the levels of ROS, TNF-α, IL-1 β and IL-6 （ P 〈 0. 05）. Conclusions To prevent LPS-induced impairment of HUVEC, tBHQ can decrease the levels of ROS inflam- matory factors induced by LPS via inducing translocation of Nrf2.

关 键 词：叔丁基对苯二酚 转录因子NF—E2相关因子2 脂多糖 人脐静脉内皮细胞 

分 类 号：R363[医药卫生—病理学]