| 引用本文: |
孙四玉,杨冬梅,戴娜,夏伯候,庹勤慧.乙酰水杨酸姜黄素酯对血管紧张素II诱导的血管平滑肌细胞增殖的影响及相关机制[J].湖南中医药大学学报,2017,37(11):1222-1225[点击复制] |
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| 乙酰水杨酸姜黄素酯对血管紧张素II诱导的血管平滑肌细胞增殖的影响及相关机制 |
| 孙四玉,杨冬梅,戴娜,夏伯候,庹勤慧 |
| (湖南中医药大学药学院, 湖南 长沙 410208;湖南中医药大学医学院, 湖南 长沙 410208) |
| 摘要: |
| 目的 探讨乙酰水杨酸姜黄素酯（curcumin acetylsalicylate，CA）对血管紧张素Ⅱ（Angiotensin Ⅱ，AngⅡ）诱导的血管平滑肌细胞（vascular smooth muscle cells，VSMC）增殖的抑制作用及其相关机制。方法 建立AngⅡ诱导的VSMC增殖模型。采用MTT法、流式细胞术观察CA干预对细胞活力和周期的影响。Western blot检测其对第10号染色体同源缺失性磷酸酶张力蛋白（phosphatase and tensin homolog deleted on chromosome ten，PTEN）、磷酸化AKT（p-AKT）、AKT蛋白表达的影响。结果 1、3、10 μmol/L CA可以显著抑制AngⅡ诱导的细胞活力，其中3 μmol/L为最佳浓度（P<0.05）。在CA的干预下，与AngⅡ组比较，流式细胞术显示VSMC G0/G1期细胞数量明显增加，S期明显减少；Western blot显示其可以促进PTEN蛋白表达，从而抑制AKT激活（P<0.05）。结论 CA可以抑制AngⅡ诱导的VSMC增殖，其机制与阻滞VSMC G0/G1期向S期转化，以及调节PTEN/AKT信号通路有关。 |
| 关键词: 乙酰水杨酸姜黄素酯 血管紧张素II 血管平滑肌细胞增殖 PTEN AKT |
| DOI：10.3969/j.issn.1674-070X.2017.11.013 |
| 投稿时间：2017-05-25 |
| 基金项目:国家自然科学基金项目（81673722）；湖南省杰出青年基金（14JJ1024）；省自然科学基金（2015JJ2117）；湖南省教育厅重点项目（16A156）。 |
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| Effect and Mechanism of Curcumin Acetylsalicylate on Angiotensin II Induced Proliferation in Vascular Smooth Muscle Cells |
| SUN Siyu,YANG Dongmei,DAI Na,XIA Bohou,TUO Qinhui |
| (School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;Medical School, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To investigate the effect and mechanism of curcumin acetylsalicylate (CA) on Angiotensin Ⅱ (AngⅡ) induced proliferation in vascular smooth muscle cells (VSMC). Methods VSMC proliferation model was induced by AngⅡ. Flow cytometry was used to observe the effect of CA on cell proliferation and cycle. The expressions of PTEN, p-AKT and AKT was detected by Western blot. Results 1, 3, 10 μmol/L CA led to a significant inhibition of Ang Ⅱ-induced proliferation of VSMCs and 3 μmol/L CA was proved to be an optimal inhibitory concentration (P<0.05). Flow cytometry showed that the number of cells in G0/G1 phase increased significantly and the number of S phase decreased significantly by the intervention of CA. Western blot showed that it could promote the expression of PTEN protein and inhibit the activation of AKT (P<0.05). Conclusion CA can obviously inhibit the VSMC proliferation induced by AngⅡ, and its mechanism is related to the inhibition of transformation from G0/G1 phase to S phase and the regulation of PTEN/Akt signaling pathway. |
| Key words: curcumin acetylsalicylate angiotensin II vascular smooth muscle cells proliferation PTEN AKT |
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