Effect of amlodipine besylate combined with Shexiang Baoxin Pill on angiotensin II-induced proliferation of aortic vascular smooth muscle cells via MAPK/ERK signaling pathway

Background and objective As disorders affecting the circulatory system, the development of cardiovascular diseases demonstrates a strong association with the aberrant biological activities exhibited by vascular smooth muscle cells (VSMCs). The present work was designed to explore the influence exerted by amlodipine besylate (AMB) combined with Shexiang Baoxin pill (SXBXP) on the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signaling cascade, and to evaluate its suppressive effect regarding angiotensin II (Ang II)-driven proliferative responses in aortic VSMCs. Materials and methods Primary aortic VSMCs were stimulated with 10 −7 mol/L Ang II and divided into the following groups: control group (154 mmol/L saline), A group (1.3 μmol/L AMB solution), B group (1% (w/v) SXBXP solution), and C group (1.3 μmol/L AMB combined with 1% (w/v) SXBXP solution). Cell proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while the cell cycle changes of VSMCs were evaluated using flow cytometry. Furthermore, the relative expression levels of p-MAPK and p-ERK were detected using Western blotting. Results Pre-treatment, the aortic VSMC growth in all groups exhibited a ‘peak-valley’ pattern. The absorbance (OD) values were lower in A group, B group and C group versus control group ( p < 0.05). The inhibition rate in C group was markedly superior to A group and B group ( p < 0.05). The proportion of cells in the G0/G1 phase in C group was the highest ( p < 0.05). Post-treatment, the relative expression levels of p-MAPK and p-ERK in A group, B group and C group were significantly lower than those in control group ( p < 0.05). Conclusion Combined treatment with AMB and SXBXP significantly inhibits Ang II-induced VSMC proliferation, which is associated with downregulation of the MAPK/ERK signaling pathway.