活血潜阳胶囊对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖的影响

Effect of Huoxue Qianyang Capsule on Cell Proliferation Induced by Angiotensin Ⅱ in Cultured Smooth Vascular Muscle Cells

目的 :观察活血潜阳胶囊对血管紧张素Ⅱ (ATⅡ )诱导的血管平滑肌细胞 (VSMC)增殖的影响。方法 :贴块法行SD大鼠胸主动脉VSMC分离培养。倒置相差显微镜、透射电镜、α SM actin鉴定。以血清药理学方法进行实验 ,采用通法采集药物血清 ,10 - 6 mol/LATⅡ为刺激因子 ,卡托普利 (Captopril)为对照 ,活血潜阳胶囊药物血清分为 10 %、7 5 %、5 %、2 5 %共 4个浓度。采用结晶紫染色法观察细胞生长曲线 ,测定氚标 -胸腺嘧啶核苷 (3H TdR)掺入量了解DNA合成的变化 ,并用透射电镜观察细胞超微结构的改变。结果 :(1)经活血潜阳胶囊处理后 ,细胞增殖速度明显下降 ,生长曲线下移 ,3H TdR掺入量减少 ,DNA合成明显受到抑制 ,其作用与Captopril相当 ,且在一定范围内有剂量依赖性。 (2 )活血潜阳胶囊可以改善ATⅡ引起的细胞超微结构改变 ,使VSMC仍保持收缩型的特征 ,与Captopril的作用相似。结论 :活血潜阳胶囊能抑制ATⅡ引起的VSMC增生和结构改变 ,从细胞水平初步探讨了活血潜阳胶囊改善高血压血管重构的机理。

Objective: To observe the effect of Huoxue Qianyang Capsule (HXQYC) on cell proliferation induced by angiotensin Ⅱ (ATⅡ) in cultured rat′s thoracic vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from the media of SD rat′s thoracic aorta obtained by explant method, and identified by inverted phase light and transmission electron microscopic (TEM) examination and immunocytochemistry assay (α SM actin). The experiment was carried out with the serum pharmacological method, with the drug contained serum gathered by 3d 2t 1hr way, the ATⅡ (10 -6 mol/L) to induce cell proliferation, as well as Captopril as drug for positive control. The concentration of HXQYC contained serum used in the experiment was 10%, 7.5%, 5% and 2.5%. The cell growth curve was observed by crystal violet staining technique, the change of DNA synthesis was evaluated by 〔 3H〕 thymidine incorporation method and the ultrastructure of cells was observed by TEM. Results: (1) After HXQYC treatment, the cell proliferation lowered significantly, the cell growth curve moved down, 3?H TdR incorporation reduced and DNA synthesis inhibited significantly. The effect of HXQYC was equivalent to Captopril and was dose dependent to a certain extent. (2) HXQYC could improve the ATⅡ induced ultrastructural change of cells, and keep VSMCs in characteristics of contractive type. The effect was similar to that of Captopril. Conclusion: HXQYC could antagonize the proliferational and structural change of VSMCs induced by ATⅡ. This article explores the mechanism of HXQYC in improving vascular reconstruction in hypertension from the cytological level preliminarily.