| The coronary heart disease is a common disease, which severely threatens human health and affects the life quality of patients in varying degrees. There are various treatments used for the treatment of coronary heart disease including pharmacological agents, percutaneous transluminal coronary angioplasty and coronary artery bypass grafting. Among them, the angioplasty is an effective minor-wounded method for coronary heart disease. Unfortunately, the incidence of restenosis which is confirmed with xoronaty angiongrahy over the first six months following angioplasty remains 30%~50%. This becomes the principal factor limiting the long-term benefit of coronary angioplasty. Pathological studies have suggested that restenosis is mainly correlated to the vessel chronic elastic recoil, the thrombus formation in sites, the migration and proliferation of vascular smooth muscle cells (VSMCs), and the excessive synthesis of extracellular matrix. Cells in the restenostic plaques were mainly composed of VSMCs Neointimal hyperplasia was formed by VSMCs migration from vessel media to subendothelium and proliferation. Therefore, it is a key step to suppress VSMCS proliferation for preventing restenosis. It was proved that the process of cells proliferation was bound to follow by cells apoptosis in cytology. If the apoptosis of VSMCs is induced in the duration of restenosis, the neointimal formation will be decreased. In the end restenosis is perverted. Arsenic trioxide(As2O3) is a much better agent used for induction of acute promyelocytic leukemia remission so far, via suppressing gene bcl-2 expression to induce leukemia cells apoptosis. Gene bcl-2 extends cells viability, whereas gene bax which belongs to bcl-2 extended family antagonizes gene bcl-2. And cells apoptosis is found in human atherosclerosis plaque and in the process of restenosis .We wondered whether AS2O3 maybe prevents restenosis after angioplasty. So we conducted the initial experiment ofAs2o3 on prevention of restenosis. The effect of AS2O3 on VSMCs growth in vitro was observed. It was shown that VSMCs growth was suppressed by As2O3 with correlation to its concentration and the reaction time, especially marked in 72h with last concentration of 3.0~4.0umol/L As2o3, by using 3-(4,5-dimethylthiazolzy)-2,5-diphenyl tetrazolium bromide chromatometry analysis. The morphology of the apoptotic cells and its transformation were observed under electron microscope. The typical DNA ladder was appeared in the DNA fragments isolated from the apoptotic cells, which indicated that the DNA was splited by endonuclease between the nucleosome subunits. The value of diploid peak before GI was larger in the higher concentration and longer time of arsenic trioxide on floe cytometry.Gene bcl-2 prolongs cells viability, while gene bax counteracts bcl-2 to induce cells apoptosis. Occurrence of cell apoptosis or not was regulated by the intracellular proportion of bcl-2 protein and bax protein. Two molecules of bax proteins can form bax homodimers to induce apoptosis. With an increase in bcl-2 protein, more bax homodimers were separated and conjugated with bcl-2 protein to form more stable bcl-2/bax heterodimers than bax homodimers, which neutralize apoptosis induction of bax protein.The results suggested that As2O3 induced VSMCs apoptosis to inhibit restenosis after artery injury, via downregulation of gene bcl-2 expression and upregulation of gene bax expression, or correlation to change of bcl-2/bax protein ratio.
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