Qin Xu-Ping, Ye Feng, Hu Chang-Ping, Liao Duan-Fang, Deng Han-Wu, Li Yuan-Jian
Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, China.
Eur J Pharmacol. 2004 Mar 19;488(1-3):45-9. doi: 10.1016/j.ejphar.2004.02.010.
The present study was designed to examine the effect of calcitonin gene-related peptide (CGRP) on angiotensin II-induced proliferation of cultured rat vascular smooth muscle cells. Vascular smooth muscle cells were grown from explants of Sprague-Dawley rat aorta. Vascular smooth muscle cells (between passages 5 and 10) were incubated with 0.1% neonatal calf serum for 48 h, and then treated with angiotensin II (100 nM) in the absence or presence of CGRP for 24 h. The viability, DNA synthesis and cell cycle of vascular smooth muscle cells were measured. Western blotting was used to determine the activity of intracellular extracellular regulated kinase (ERK1/2). Angiotensin II significantly decreased the viability and proliferation of vascular smooth muscle cells, decreased the proliferation index, and increased the activity of ERK1/2; the effects of angiotensin II were inhibited by CGRP (1-100 nM) in a concentration-dependent manner. In conclusion, CGRP significantly inhibits angiotensin II-induced proliferation of vascular smooth muscle cells, an effect related to a decrease in the activation of mitogen-activated protein kinase pathway.
本研究旨在探讨降钙素基因相关肽（CGRP）对血管紧张素II诱导的大鼠血管平滑肌细胞增殖的影响。血管平滑肌细胞取自Sprague-Dawley大鼠主动脉外植体。将第5至10代的血管平滑肌细胞用0.1%新生牛血清孵育48小时，然后在不存在或存在CGRP的情况下用血管紧张素II（100 nM）处理24小时。检测血管平滑肌细胞的活力、DNA合成和细胞周期。采用蛋白质免疫印迹法测定细胞外调节蛋白激酶（ERK1/2）的活性。血管紧张素II显著降低血管平滑肌细胞的活力和增殖，降低增殖指数，并增加ERK1/2的活性；CGRP（1-100 nM）以浓度依赖的方式抑制血管紧张素II的作用。总之，CGRP显著抑制血管紧张素II诱导的血管平滑肌细胞增殖，这一作用与丝裂原活化蛋白激酶途径激活的降低有关。
