RhoA/ROCK信号系统对血管外膜炎症介导的大鼠颈动脉平滑肌细胞增殖和表型变化的影响

 目的 探讨RhoA/ROCK信号系统在血管外膜炎症介导的大鼠颈动脉平滑肌细胞（VSMC）增殖和表型变化中的作用机制。 方法 将20只Wistar大鼠按随机数字表法均分为模型组（用硅胶管包裹大鼠颈动脉1周，造成血管外膜的慢性炎性损伤）和对照组，取材后HE染色，分别观察2组血管形态学变化，采用RT-PCR和Western blot检测血管组织中SM α-actin 与ROCK2的表达。 结果 与对照组相比，模型组颈动脉血管外膜增厚，炎性细胞浸润，中膜平滑肌细胞增生，排列紊乱，VSMC中SM α-actin mRNA水平和蛋白表达水平均增高，ROCK2 mRNA水平与对照组相比无显著差异，蛋白表达水平均明显增高。 结论 RhoA/ROCK信号系统可能参与血管外膜炎症介导的大鼠颈动脉VSMC增殖和表型变化的调控。

Effects of RhoA/ROCK Signaling Pathway on the Proliferation and Phenotypic Modulation of Vascular Smooth Muscle Cells in Perivascular Inflammatory Injured Rat Carotid Artery

Objective To investigate the role of RhoA/ROCK signaling pathway in the proliferation and phenotypic modulation of vascular smooth muscle cells in perivascular inflammatory injured rat carotid artery.Methods A total of 20 Wistar rats were randomly divided into 2 groups as model group and control group.Bilateral carotid artery model with chronic inflammatory injury was established by silicone collar which was positioned around the carotid artery adventitia of the rat.After operation,the rats were fed with standard food and free water for 7 days.Carotid artery specimens was obtained for HE staining to evaluate the vascular morphological changes.Western blot was used to detect the expression of vascular tissue SM α-actin and ROCK2 protein;RT-PCR method was applied to detect mRNA expression of vascular tissue SM α-actin and ROCK2.Results Compared with the carotid artery of control rats,the thicker adventitia and adventitial inflammation was observed in the model group;the intima smooth muscle cells significantly proliferated and arranged in disorder.Compared with control group,carotid artery vascular smooth muscle cell SM in model group had higher α-actin expression at both mRNA and protein level;no significant difference of ROCK2 mRNA expression was observed between 2 groups,however,the protein expression was significant higher in model group.Conclusion RhoA / ROCK signaling pathway may be involved in the proliferation and phenotypic modulation of vascular smooth muscle cells in perivascular inflammatory injured rat carotid artery.