L-精氨酸对大鼠血管球囊损伤后病理学变化的影响

Effects of L-arginine on the pathological changes after vascular balloon injury in rats

目的:探讨Ｌ－精氨酸(Ｌ－Arg)对大鼠血管球囊损伤后病理学变化,细胞周期依赖性激酶2(CDK２)、细胞周期蛋白E(CyclinE)、增殖细胞核抗原(PCNA)的表达和血小板颗粒膜蛋白(GMP－140)、D－二聚体(D－dimer)含量的影响。方法:63只大鼠,随机分为对照组(n＝7),手术组(n＝28)和Ｌ－Arg组(n＝28),监测以上各项指标。结果:①对照组动脉腔内无新生内膜;手术组动脉腔内有明显新生内膜;Ｌ－Arg组新生内膜明显减轻。新生内膜面积及内膜/中膜面积,Ｌ－Arg组较手术组分别降低59．1%及62．9%(均为P＜0.01)。②对照组COK2、CyclinE和PCNA表达呈阴性,手术组均呈强阳性,Ｌ－Arg组表达减少。③手术组血浆NO水平低于对照组及Ｌ－Arg组(P均＜0．01),而血浆GMP-140和D-dimer显著高于对照组(P＜0．001)和Ｌ－Arg组(P＜0．01)。④血浆GMP-140与D－dimer含量与新生内膜面积及内膜/中膜面积比均呈显著正相关,r分别为0.89(P＜0.01)、0.86(P＜0．05)和0.79、0．84(P＜0．05)。结论:Ｌ－Arg能有效抑制血管内膜损伤后的内膜增生,其机制可能与逆转CDK2、CyclinE的过度表达和抑制血小板活化、血栓形成有关。

Aim :To investigate the effects of L-Arg on the pathological changes, the expressions of CDK2, CyclinE, PCNA, and the contents of serum GMP-140 and D-dimer after vascular balloon injury in rats. Methods: Sixty-three rats were randomly allocated into 3 groups: Control group (group C, n = 7) , Operation group (group 0, n = 28 ) , and L-Arg group (group L, n= 28). The indexes mentioned above were examined. Results: ① Vascular lamina surface in group C was smooth; evident neointima was observed in group O; in group L the neointima was less obvious than that in group O.②CDK2,CyclinE and PCNA were negatively expressed in group C, but positively expressed in group O. In group L, the expressions of those indexes decreased. ③The content of plasm NO in group O was lower compared with those in group C and group L( P < 0.001). The contents of GMP-140 and D-dimer were higher after balloon injury in group O compared with those in group C (P < 0.001) and group L (P < 0.01).④ The contents of GMP-140 and D-dimer were positively associated with the neointima area and the ratio of intima area to tunica media area. The correlation coefficients were 0.89( P < 0.01) ;0.86( P < 0.05) ;0.79( P < 0.05) ;0.84( P < 0.05), respectively. Conclu-sion: L-Arg can evidently inhibit the increase of neointima after vascular balloon injury. The mechanism may be associated with reversing over-expressions of CDK2 and CyclinE, and inhibiting platelet activation and thrombosis formation.