| Objective:90 percent of the heart interstitial cell is the cardiac fibroblast,which is very important during the normal growth and the pathological remodeling of the heart.The anormal proliferation of the cardiac fibroblast can facilitate the progress of the remodeling of the cardiac ventricle and accelerate the process of the heart failure.So,using drugs to inhibiting the anormal proliferation and accelerating the process of CFs senescence will postpone the process of the heart fibrosis. Captopril is used widesperadly in clinic.It has been proved that captopril could postpone the heart fibrosis,improve the cardiac ventricle remodeling and arrest the progress of the heart failure.But the molecular mechanism has not been known.Our experimental objective is to observe the effect of captopril on the heart fibroblast cell senescence of suckling mice,and identify if Cap will accelerate the process of CFs senescence.To identify the mechanism of captopril postponing the heart fibrosis and improving the cardiac ventricle on the cellular level.Methods:The cardiac fibroblast cells of SD immature rats through primary culture have been purified to heart fibroblast cells through three passage.Our experiment selected three to seven generation cells,and used 1mg/l,5mg/l and 10mg/l captopril influencing CFs for 72 hours respectively.We detected the telomeres length with flow cytometry fluorescence in situ hybridization (Flow-Fish); observed these cells with the senescence-relatedβ-galactosidase staining;detected cell life cycle of CFs with flow cytometry; observed the mitochondria damage of each CFs group with electronic microscope.Apart from this,we used 10g/L D-gal to influence CFs 72h and established the CFs senescence model.We gave this model 1mg/l captopril and detected the cellular SOD activity,content of MDA.Then we detected cell life cycle of CFs with flow cytometry and the telomeres length with flow cytometry fluorescence in situ hybridization(Flow-Fish).Results:... |
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