摘要
目的观察缬沙坦（Val）对血管紧张素1I（AngⅡ）刺激下大鼠胸主动脉血管平滑肌细胞（VSMCs）的增殖与迁移及对p-ERK1／2、P—P38表达的影响。方法组织贴块法培养VSMCs，取3～5代细胞进行实验。采用MTT法检测Val对AngⅡ诱导下细胞增殖的影响，采用划痕试验法进行细胞迁移实验，采用蛋白质印迹法检测VSMCs中ERK1／2、PERK1／2、P38、p-P38的表达。结果（1）Angll能明显促进VSMCs的增殖，AngⅡ促进VSMCs增殖的作用能被Val和PD98059所抑制，并且Val呈浓度依赖性抑制VSMCs增殖。SB23015能明显促进VSMCs增殖。（2）细胞经AngⅡ作用后，迁移活性明显增加，Val及PD98059抑制AngⅡ诱导的大鼠VSMCs迁移，但SB23015作用与之相反。（3）Va1和PD98059能抑制AngⅡ的促VSMCs胞内PERKl／2表达的作用，而SB23015则能增强这种作用。Val和SB23015能抑制AngⅡ的促VSMCs胞内PP38表达的作用，而PD98059则对此无显著影响。（4）Val单独作用于VSMCs时，对细胞的增殖、迁移及P～ERK1／2、P—P38的表达均无明显影响。结论（1）Val呈浓度依赖性抑制AngII诱导VSMCs的增殖和迁移。（2）Val抑制AngⅡ诱导VSMCs的增殖和迁移与其抑制AngⅡ诱导的PERK1/2的表达相关。（3）P—P38对AngⅡ诱导的p—ERK1／2的激活起负调节作用。
Objective To investigate the effect of valsartan on the proliferation and migration of rat aortic smooth muscle cells and the expression of p-ERK1/2, p-P38 promoted by angiotensinII （Ang II ）. Methods VSMCs from the rat thoracic aorta were cultured by attachment-block culture. VSMCs from3-5 passages were used. The proliferation of VSMCs was tested by MTT meth- od. Pipettetip wounding injury was used to access the migration of VSMCs. The expression of ERK1/2 ,p-ERK1/2, P38 and p-P38 of VSMCs was detected by Western Blot. Results （1） Ang II could significantly promote the proliferation of VSMCs. The prolifer- ation of VSMCs promoted by Ang II could be inhibited by Valsartan and PD98059. Vaisartan inhibited the proliferation of VSMCs in a concentration-dependence. SB23015 could significantly promote the proliferation of VSMCs. （2）The migration activity of VSMCs in the Ang III was increased significantly. Valsartan and PD98059 inhibited Ang II induced migration of rat VSMCs and SB23015 was on the contrary. （3） Valsartan and PD98059 could inhibit Ang II-induced VSMCs intracellular p-ERK1/2 protein ex- pression,and this role was enhanced by SB23015. Valsartan and SB23015 could inhibit Ang H-induced VSMCs intracellular p-P38 protein expression, and PD98059 had no significant effect. （4）VSMCs had no significant effect on cell proliferation, migration and p- ERK1/2, p P38 protein expression under valsartan alone. Conclusion （1）Valsartan could inhibit Ang II -induced proliferation and migration of VSMCs in a concentratiowdependenee. （2）The effects that valsartan inhibits the proliferation and migration of Ang II- induced VSMCs might be related to its inhibiting Ang II-induced p ERK1/2 protein expression. （3）p P38 might play a negative reg- ulatory role on the Ang II-induced p-ERK1/2 activation.
出处
《重庆医学》
CAS
CSCD
北大核心
2014年第7期830-833,共4页
Chongqing medicine
关键词
肌
平滑
血管
血管紧张素Ⅱ
冠心病
P38丝裂原活化蛋白激酶
muscle, smooth, vascular
angiotensin II
coronary diseas
P3 8 mitogen-activated protein kinases
