Study On The Effects Of Astragalus And Angelica Compatibility On The Proliferation Of VSMCs In Rat Vascular Intimal Hyperplasia And The Mechanism Of PI3K/Akt Signaling Pathway

AIM To investigate the effect of different Astragalus-Angelica compatilibity on intimal hyperplasia,and to establish the effective compatibility of Astragalus-Angelica against intimal hyperplasia.Further more,based on the effective compatibility of Astragalus-Angelica,the effects of Astragalus-Angelica on phenotype transformation,cell proliferation cycle and cell proliferation relating PI3K/Akt signaling pathway of vascular smooth muscle cells(VSMCs)in proliferated intima were investigated.Methods A model of intimal hyperplasia of thoracoabdominal aorta was established by balloon catheter injury in male Sprague-Dawley rat,and the model rats were administrated Astragalus and Angelica with single use or different ratios for 14 days by means of intragastric administration.Then the thoracoabdominal aorta was taken out and masson staining was used to analyze the pathological changes of the Neointima.The expression of cell cycle relating cyclin D1、cydlin E proteins and cell proliferation relating PI3K/Akt signaling pathway PI3K、Akt proteins in hyperplastic intima is also analysed.Results After balloon injury of aortic endothelium,VSMCs phenotype transformation and proliferation can be induced,resulting in intimal hyperplasia.In hyperplastic intima,the expression of SM-actin can be enhance and the expression of PCNA can be inhibited by the Astragalus and Angelica with single use and Astragalus-Angelica of 1:1 and 5:1 combination.The increased expression of cyclinD1 or cyclinE proteins in damaged blood vessels,and p-PI3 K or p-Akt proteins in hyperplastic intima can be inhibited by the Astragalus and Angelica with single use and Astragalus-Angelica of 1:1 and 5:1 combination.Conclusion Vascular intimal hyperplasia can be inhibit by Astragalus-Angelica compatilibity,and the Astragalus-Angelica 1:1 compatibility has the strongest effect.Its effect is related to the inhibition of the phenotype transformation and VSMCs proliferation after vascular endothelial damage.The mechanism may be related to the inhibition of the activation of PI3K/Akt signaling pathway,then inhibite the proliferation of VSMCs.