【摘要】 目的观察脱氢表雄酮(DHEA)对血管平滑肌细胞(VSMC)氧化应激损伤中核转录因子(NF-κB)的表达干预作用。方法贴块法培养雄性SD大鼠胸主动脉血管平滑肌细胞,实验分四组A组(对照组)、B组(50μmol/LH2O2处理6h)、C组(50μmol/LH2O2+1nmol/LDHEA处理6h)和D组(50μmol/LH2O2+10nmol/LDHEA处理6h)。免疫细胞化学法分析核因子p65(NF-κBp65)核易位情况。结果B组VSMCNF-κBp65的核易位阳性率显著高于A组;而与B组相比,C组和D组VSMCNF-κBp65的核易位阳性率显著降低,其中D组降低更为明显。结论DHEA能显著抑制H2O2引起VSMCNF-κB的激活,这可能是DHEA延缓动脉粥样硬化形成的机制之一。更多还原

【Abstract】 Objective To observe the effect of dehydroepiandrosterone (DHEA) intervention on the expression of NF-κB induced by oxidative stress damage in vascular smooth muscle cells (VSMCs).Methods VSMCs cultured from thoracic aorta of male Wista rats by explant method were divided into group A (control), group B(6 h intervention of 50μmol/L H2O2), group C (6 h intervention of 50μmol/L H2O2 +1 nmol/L DHEA) and group D (6 h ntervention of 50μmol/L H2O2 +10 nmol/L DHEA). Immunocytochemical method was employed to evaluate the nuclear translocation of NF-κB subunit p65.Results The nuclear translocation of NF-κB p65 in VSMCs in group B was significantly higher than that in group A, C and D, especially in group D.Conclusions DHEA could significantly inhibit the activation of NF-κB induced by H2O2 in VSMCs, which might be the one of mechanisms for delaying atherogenesis by DHEA.更多还原