摘要
目的研究金雀异黄素对氧化型低密度脂蛋白诱导的人血管平滑肌细胞中核因子κB激活的影响,并对其作用机制进行初步探讨。方法以体外培养的人脐静脉平滑肌细胞为对象,用50 mg/L的氧化型低密度脂蛋白作用细胞2 h,并加入不同浓度金雀异黄素(10,30,90 mol/L)对其进行干预,免疫细胞化学方法检测各组血管平滑肌细胞中核因子κB亚单位p65核移位阳性细胞数,Western blot法检测细胞内κB抑制蛋白-α含量变化,硝酸还原酶法测定各组细胞培养液中一氧化氮生成量。结果人脐静脉平滑肌细胞经氧化型低密度脂蛋白刺激2 h后,其核移位阳性细胞数为76.67±3.21,与空白组1.33±0.58相比明显增加(P<0.01),再与不同浓度金雀异黄素共同孵育2 h后,核移位阳性细胞数分别为28.33±2.52,19.67±1.53和15.67±2.89,与单纯给予氧化型低密度脂蛋白刺激相比明显减少(P<0.01),且随着浓度升高有递减的趋势;30,90μmol/L金雀异黄素能明显增加细胞内κB抑制蛋白-α的含量;各组细胞培养液内的一氧化氮生成量差异无显著性。结论金雀异黄素能抑制氧化型低密度脂蛋白诱导的血管平滑肌细胞中核因子κB的活化;其作用机制可能涉及增加细胞内κB抑制蛋白含量,未发现与一氧化氮有关。
Aim To investigate the effect of genistein on activation of nuclear factor kappa B （ NF-κB ） in vascular smooth muscle cells （VSMC） induced by oxidized low density lipoprotein （ox-LDL） and further examine the activation mechanism. Methods Human umbilical vein smooth muscle cells were pretreated with genistein in different concentrations （ 10, 30, 90 μmol/ L） and then treated by 50 mg/L of ox-LDL for 2 hours. Immunocytochemistry staining was used to detect the nuclear translocation of NF-κB subunit p65. The intracellular level of inhibitory kappa B （ IκB ） , inhibitor of NF-κB, was detected by Western blotting analysis. The levels of nitric oxide （NO） in the culture medium was detected by the method of nitric acid reductase. Results Genistein significantly restrains the nuclear translocation of NF-κB in VSMC induced by ox-LDL ; High concentration of genistein increases intracellular IκB-α level and doesn＇ t have significant effect on level of NO in the culture medium. Conclusion Genistein inhibited activation of NF-κB induced by ox-LDL in VSMC. The mechanism is associated with increase of κB and may not associate with nitric oxide level.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2009年第5期363-366,共4页
Chinese Journal of Arteriosclerosis
基金
贵州省教育厅基金项目(黔教科2006314)
遵义医学院硕士启动基金(2005-015)
