Yang Xiao-fang, Xiong Jian-wen, Wang Zhi-lu, Li Yan, Xu Zhe-tong, Cui Li-jun, Wang Feng, Tan Li-li, Zhang Li
Department of Cardiology, First Hospital of Lanzhou University, Key Lab of Preclinical Study for New Drugs of Gansu Province, Lanzhou 730000, Gansu, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2009 Nov;21(11):656-9.
To explore the protective effect of erythropoietin (EPO) against oxidized-low density lipoprotein (ox-LDL)-induced apoptosis in human umbilical vein endothelial cells (HUVECs) in an ox-LDL induced apoptosis model.
Third-sixth passage of cultured HUVECs were used, and they were divided into two groups. The cells were pretreated with different concentrations (6.25, 50, 100 kU/L) of recombinant human erythropoietin (rhEPO) for 24 hours, then they were exposed to ox-LDL (100 mg/L) for 48 hours; another group of cells were pretreated with antisense to 0.5 micromol/L LOX-1 mRNA or 0.5 micromol/L sense for 24 hours, and then HUVECs were exposed to ox-LDL (100 mg/L) for 12 hours. Apoptosis was assessed by the apoptosis ratio, cell viability, and Bcl-2/Bax ratio.
As compared to untreated controls, pretreatment with rhEPO led to increased cell survival of HUVECs and decreased cell apoptosis in a dose-dependent manner (all P<0.05). Consistently, the Bcl-2/Bax ratios were also increased in a similar fashion. The ratio of apoptosis protein Bcl-2/Bax was increased in the antisense LOX-1 mRNA group than that of ox-LDL group (P<0.05), but the one in the sense LOX-1 mRNA group was not significantly different from that of ox-LDL group.
The ox-LDL can induce apoptosis in HUVECs by regulating LOX-1 mRNA, and rhEPO can increase Bcl-2/Bax ratio and inhibit ox-LDL-induced apoptosis of HUVECs.
在氧化型低密度脂蛋白（ox-LDL）诱导的细胞凋亡模型中，探讨促红细胞生成素（EPO）对人脐静脉内皮细胞（HUVECs）氧化型低密度脂蛋白诱导的细胞凋亡的保护作用。
使用培养的第3至6代HUVECs，将其分为两组。细胞用不同浓度（6.25、50、100 kU/L）的重组人促红细胞生成素（rhEPO）预处理24小时，然后暴露于ox-LDL（100 mg/L）48小时；另一组细胞用0.5 μmol/L LOX-1 mRNA反义核酸或0.5 μmol/L正义核酸预处理24小时，然后将HUVECs暴露于ox-LDL（100 mg/L）12小时。通过凋亡率、细胞活力和Bcl-2/Bax比值评估细胞凋亡。
与未处理的对照组相比，rhEPO预处理导致HUVECs细胞存活率增加，细胞凋亡减少，呈剂量依赖性（均P<0.05）。同样，Bcl-2/Bax比值也以类似方式增加。反义LOX-1 mRNA组凋亡蛋白Bcl-2/Bax比值高于ox-LDL组（P<0.05），但正义LOX-1 mRNA组与ox-LDL组无显著差异。
ox-LDL可通过调节LOX-1 mRNA诱导HUVECs凋亡，rhEPO可增加Bcl-2/Bax比值并抑制ox-LDL诱导的HUVECs凋亡。
