Du Xiao-Dong, Zhang Shu, Cao Yu, Nie Hu
Emergency Department, West China Hospital, Sichuan University, Chengdu, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2009 Sep;40(5):826-8.
To investigate the possible mechanism of felodipine on experimental atheroselerosis formation in rats.
The rat model of atherosclerosis was established by the methods of intraperitoneal injection of Vitamin D3 and high-fat diet. Thirty male SD rats were randomly divided into normal group, atherosclerosis model group and felodipine treating group. At the end of 6 weeks, the expression of NF-kappaB (nuclear transcription fator-kappaB) in endothelial cells and smooth muscle cells of aorta were determined.
The positive rates of NF-kappaB in both atherosclerosis model group and felodipine treating group (46.59+/-5.68, 20.47+/-1.97) were higher than that of normal group (4.38+/-1.07, P<0.01). The expression of NF-kappaB in atherosclerosis model group was higher than that of felodipine treating group (P<0.01).
The mechanism of felodipine in relieving atheroselerosis may correlate with the inhibition of NF-kappaBp65 activation.
探讨非洛地平对大鼠实验性动脉粥样硬化形成的可能机制。
采用腹腔注射维生素D3和高脂饮食的方法建立大鼠动脉粥样硬化模型。30只雄性SD大鼠随机分为正常组、动脉粥样硬化模型组和非洛地平治疗组。6周结束时，测定主动脉内皮细胞和平滑肌细胞中核转录因子κB（NF-κB）的表达。
动脉粥样硬化模型组和非洛地平治疗组NF-κB阳性率（46.59±5.68，20.47±1.97）均高于正常组（4.38±1.07，P<0.01）。动脉粥样硬化模型组NF-κB表达高于非洛地平治疗组（P<0.01）。
非洛地平缓解动脉粥样硬化的机制可能与抑制NF-κBp65激活有关。
