【摘要】 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。更多还原

【Abstract】 To observe the roles of Gαq/ 11 mediated- and platelet-derived growth factor (P[)GF) mediated-signal transduction pathways in proliferation and migration of vascular smooth muscle cells (VSMC) after arte-rial injury, a vascular cell proliferation model was established by balloon injury in rat aorta and the morphologic changes in injured vascular walls after the injury were studied. Activities of angiotensin converting enzyme (ACE) and aorta phospholipase C (PLC) were tested, and levels of platelet-derived growth factor receptor-n (PDGFR-β) and Gαq/ 11 protein were measured by Western blot analysis. At 1 day after operation, injured aortic segments showed denudation in endothelial cells. Medial VSMC proliferation and intimal hyperplasia were not observed. As compared with the sham group, ACE activities were increased by 382.7% (P <0.01), but the expression of PDGFR-β and PLC activities did not show significant changes (P > 0.05). In addition, the level of Gαq/1 1 protein was decreased by 20.0% (P <0.05). At 14 days after operation, sections of in-jured aorta showed marked intimal thickening with large numbers of VMSCs proliferating throughout intima and media. In comparison with the sham group, ACE activity, PLC activity and the level of PDGFR-β were in-creased by 420.2% (P<0.01), 186.2% (P<0.05) and 85.0% (P<0.05), respectively. While the level of Cαq/11 protein was decreased by 33. 1% (P <0.01). The above data suggest that the PDGF-mediat-ed signal transduction pathway plays an important role in VSMC proliferation.更多还原