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采用大鼠主动脉球囊内皮剥脱术制备主动脉狭窄模型，观察Ｇαｑ／１１和ＰＤＧＦ信号转导通路在大鼠主动脉球羹损伤后狭窄时血管平滑肌细胞（ＶＳＭＣ）增殖和迁移中的作用。实验分假手术组、损伤１ｄ组和损伤 １４ ｄ组，观察形态学变化，检测血管紧张不转换酶（ＡＣＥ）活性和主动脉磷脂酶Ｃ（ＰＬＣ）活性，用免疫印迹法测定主动脉血小板源生长因子（ＰＤＧＦ）受体β和 Ｇαｑ／１１蛋白含量。结果显示：损伤 １ｄ，主动脉内皮完全剥脱，ＶＳＭＣ无明显增殖和迁移，内膜无增厚。与假手术组比较．ＡＣＥ活性增加３８３．７％（Ｐ＜０．０１），ＰＤＧＦ受体β表达和ＰＬＣ活性无明显变化，Ｇαｑ／１１蛋白含量下降２０．０％（Ｐ＜０．０５）。损伤１４ｄ组，主动脉局部有新生内皮出现，中层ＶＳＭＣ大量增殖井向内膜下迁移，内膜显著增厚。ＡＣＥ活性、ＰＤＧＦ受体β表达和ＰＬＣ活性分别较假手术组升高４２０．２％（Ｐ＜０．０１）、８５．０％（Ｐ＜０．０５）和１８６．２％（Ｐ＜０．０５），Ｇαｑ／１１蛋白表达下降３３．１％（Ｐ＜０．０１）。结果提示，ＰＤＧＦ介导的信号转导通路可能是再狭窄时ＶＳＭＣ增殖的重要佰号转导机制。
Aortic stenosis was induced by aortic balloon angioplasty in rats. The effects of Gαq / 11 and PDGF signal transduction pathways on the proliferation and migration of vascular smooth muscle cells (VSMCs) after stenosing aortic fibers were observed. The rats in the sham operation group, the injury 1d group and the injury 14d group were observed morphological changes, ACE activity and aortic phospholipase C (PLC) activity were detected, and the aortic platelet source Growth factor (PDGF) receptor beta and Gαq / 11 protein content. The results showed that 1 day after injury, the aortic endothelium completely exfoliated, VSMC did not proliferate and migrate obviously, and there was no thickening of the intima. Compared with sham operation group. ACE activity was increased by 383.7% (P <0.01). There was no significant change in PDGF receptor β expression and PLC activity, but Gαq / 11 protein content was decreased by 20.0% (P <0.05). Injured 14d group, there is a new part of the aorta endothelium appears, a large number of middle layer of VSMC proliferation wells migrate to the intima, the intima significantly thickening. ACE activity, PDGF receptor β expression and PLC activity were increased by 420.2% (P <0.01), 85.0% (P <0.05) and 186.2% (P <0), respectively .05), Gαq / 11 protein expression decreased by 33.1% (P <0.01). The results suggest that PDGF-mediated signal transduction pathway may be an important translocation mechanism of VSMC proliferation during restenosis.