ABSTRACT
Objective To explore the effect of trimetazidine on myocardial structure injury induced by pyran adriamycin and to clarify the protective effect of trimetazidine on. the changes of myocardial structure and its mechanism.Methods 36 Wistar rats were randomly divided into control group,model group and treatment group. The rats in model group and treatment group were injected with pyran doxorubicin 2.5 mg·kg-1 (concentration 2 g·L-1 )by the caudal vein once a week.The rats in control group were injected with equivalent normal saline for 6 weeks.The rats in treatment group were intragastricly infused with trimetazidine 5.4 mg · kg · d-1 one day before making the model.The rats in control group and model group were injected with equivalent normal saline for 8 weeks.At the end of the experiment, the myocardial enzymes in serum of the rats in various groups were measured. The morphology of myocardium tissue was detected by light microscope and electron microscope. Results Compared with model group,the levels of myoglobin,troponin I and alanine transaminase (ALT)of the rats in treatment group were significantly decreased (P<0.05).Under light microscope the myocardium of the rats in model group arranged disorderly, the structure was severely damaged, emyocardial was seen, the myofilament was dissolved;the myocardium of the rats in treatment group arranged in order, the structure was nearly integrated,partial dissolution and fracture were found.Under electron microscope in model group the myocardial muscle bundle dissolved, fractured and disappeared, and the mitochondria was decreased,and the cytoplasmic matrix cavitation was seen;the cardiomyocytes sarcomeres of the rats in treatment group arranged in order,local myofilaments were reduced slightly, the surrounding mitochondria were oval and arranged in parallel between the muscle bundles.Conclusion Trimetazidine has protective effect on the cardiomyocyte injury caused by pyran adriamycin,and its mechanism may be related to decreasing the injury of mitochondria and myocytes.
ABSTRACT
Objective To study the antileukemia immune response of IL-18 gene transfected dendritic cells(DCs) of chronic myelogeous leukemia(CML).Methods DCs were transfected with IL-18 gene by liposomes in CML.The expression of IL-18 in IL-18 transfected DCs was detected.The percentages of CD80+ and CD86+ cells in IL-18 tranfected DCs were determined by FCM.The proliferation of T cell,NK and specific CTL kill activity induced by IL-18 gene transfected DCs were detected.Results The quantity of IL-18 in IL-18 tranfected DCs was(596?34.1)pg/2?106cells/48 h,while the culture medium of mock-transduced DCs and DCs did not secrete detectable levels of IL-18.The percentages of CD80+ and CD86+ cells in IL-18 tranfected DCs were higher than that in mock-transfected DCs(P
ABSTRACT
Objective To set up an effective and low-price way for enriching dendritic cells precursor from chronic myelogeous leukemia by Percoll density gradients.Methods Peripheral blood mononuclear cells(PBMCs) were collected by separation through Ficoll-Hypaque,then PBMCs were separated by 55% Percoll gradients. The cell type and DCs expressing CD1a,CD86 were detected in the high-density group(C),low-density group(B) and non-Percoll separation group(A).Results After separation of 55% Percoll,the percentage of promyelocytes and myelocytes in group B was obviously higher than those in group A and group C(P