ABSTRACT
Objective:To explore therapeutic effect and safety of cilostazol combined clopidogrel +aspirin on aged pa‐tients after percutaneous coronary intervention (PCI) .Methods :A total of 100 aged patients with coronary heart disease undergoing PCI were randomly divided into routine treatment group (n=52 ,received aspirin and clopidogrel antiplatelet therapy) and cilostazol group (n= 48 ,received cilostazol therapy based on routine treatment group ) . Turbidimetry was used to measure platelet aggregation rate (PAR );PAR and mean platelet volume (MPV ) were compared between two groups before ,one week and one month after PCI .All subjects were followed up for six months ,incidence rates of major adverse cardiovascular events (MACE) and hemorrhage events were compared be‐tween two groups .Results:There were no significant difference in MPV and PAR between two groups before PCI . Compared with routine treatment group ,PAR significantly reduced [one week after PCI :(48.7 ± 6.3)% vs .(43.5 ± 5.7)% ,one month after PCI :(46.8 ± 5.8)% vs .(42.4 ± 5.4)% ] in cilostazol group , P0.05;incidence rate of hemorrhage in cilostazol group was significantly lower than that of routine treatment group (6.25% vs .19.23% , P< 0.01) .Conclusion:Compared with clopidogrel+aspirin therapy ,cilostazol combined clopidogrel+aspirin can more significantly inhibit platelet ag‐gregation ,and significantly reduce hemorrhage events ,so they are safe and effective in aged patients with coronary heart disease undergoing PCI .
ABSTRACT
Objective To investigate the effect of tMfn2 gene on inhibiting the proliferation of vascular smooth muscle cells (VSMCs) and related mechanism. Method VSMCs were transfected with adenovirus vector encoding tMfn2 or Mfn2 (Adv-tMfn2, Adv-Mfn2). The abundance of tMfn2 protein and Mfn2 protein were deter-mined by Western blot analysis using Mfn2 N-term antibody. The effect of tMfn2 on the proliferation of VSMCs was explored by cell counting and MTT assay. The cell cycle was analyzed using flow cytometry. Western blot were used to detect the expression of p-ERK1/2 and p-Raf-1. Results The results of cell counting and MTT both indi-cated that tMfn2 gene displayed more remarkable effect on inhibiting the proliferation of VSMCs than Mfn2 (P <0.01). Flow cytometry showed that most of the cells infected with Adv-tMfn2 or Adv-Mfn2 were blocked in the stage of G0/G1 and few entered into the S phase. Western blot indicated that overexpression of tMfn2 gene resulted in downregulation of phosphorylated ERK1/2 and Raf-1 protein (P < 0.01). These results demonstrated tMfn2 had stronger effect than Mfn2 (P < 0.01). Conclusions tMfn2 gene is superior to Mfn2 gene in attenuating the proliferation of VSMCs via the Ras-Raf-ERK1/2 signaling pathway.