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AIM:To investigate the effects of atorvastatin reloading in pre-percutaneous coronary intervention ( PCI) period on endothelial progenitor cell ( EPC) count and inflammatory cytokine expression in the stable angina pectoris patients who had previously received long-term statin treatment.METHODS:The patients with stable angina pectoris that had received long-term statin therapy and planned to accept PCI were randomized into 3 groups:80 mg atorvastatin 12 h and 40 mg 2 h before coronary angioplasty (80 mg reloading), pre-operatively with 40 mg/d atorvastatin for 7 d (40 mg re-loading) , and without atorvastatin reloading ( no reloading ) .CD45 -/CD133+/CD34 +, CD45 -/CD34 +/KDR+ and CD45 -/CD144 +/KDR+EPCs in 100 μL peripheral blood were determined by flow cytometry 1 h prior to PCI and 1 h, 6 h and 24 h after PCI.The serum concentrations of soluble intercellular adhesion molecule 1 ( sICAM-1) , C-reactive protein ( CRP) and troponin I ( TnI) were analyzed immediately prior to and 24 h after PCI.RESULTS:(1) In 80 mg reloading group, the numbers of circulating CD45 -/CD133 +/CD34 +and CD45 -/CD34 +/KDR+early differentiation stage EPCs 1 h and 6 h after coronary angioplasty was significantly elevated compared with those before PCI (P<0.05).(2) In control group, the serum concentrations of sICAM-1 and CRP 24 h after PCI were significantly elevated ( P<0.05) compared with preoperative values.(3) The rise in serum TnI concentration from pre-to post-operation in 80 mg reloading group was lowerthan that in control group.CONCLUSION: The method of atorvastatin reload before PCI affects the number of EPCs inperi-operative period.High dose of atorvastatin application before PCI triggers early EPC circulation.The serum levels ofpost-operative inflammatory cytokine sICAM-1 as well as CRP are reduced by atorvastatin reloading before PCI.
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Objective To evaluate the growth inhibition of human gastric carcinoma cell lines SGC 7901 in vitro and the expression of bcl-2, bcl 2l12 and bax with docosahexaenoic acid (DHA) and 5-fluorouracil (5-FU). Methods The effect of DHA and 5-FU was measured by trypan blue, and the interaction between two agents was judged by combination index (CI). Cells were observed by inverted microscope. Flow cytometry was used for analysis of apoptosis by PI staining and Annexin-V/PI. RT-PCR was used to analyze the levels of bcl-2, bcl 2l12 and bax mRNA. Results DHA significantly inhibited the growth of SGC 7901 cells in a dose- and time-dependent way ( P < 0. 05 ), the IC50 of 24 h and 48 h was 67. 81 μg/ml and 45.76 μg/ml, and a strong synergism was found in the combination of DHA and 5-FU (CI < 1 ,P <0. 01 ). Treated by DHA and 5-FU for 48 h, cells became sparse under inverted microscope. DHA or 5-FU was able to induce apoptosis and the effect became even more significant by the combination of DHA and 5-FU. Cells were holted in phase of G01/G1 and S. RT-PCR showed that DHA or 5-FU down-regulated the expression of bcl-2 and bcl 2l12 mRNA, while bax mRNA expression was not downregnlated. Conclusions DHA could inhibit the growth of gastric carcinoma cells, DHA and 5-FU had synergetic effect in the inhibition of the cells growth and blockage of the cell cycles possibly by down-regulating the expression of bcl-2 and bcl 2l12.
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OBJECTIVE To study characteristics of changing T lymphocytes in epidemic hemorrhagic fever(EHF) patients during acute phase and find out the pathogenesis,in order to elevate the level of early diagnosis.METHODS The anticoagulant blood from 30 cases of EHF patients and 50 normal healthy blood donors was collected.T lymphocyte subsets were detected by flow cytometry.RESULTS Compared with those of normal persons,CD4+ T cell counts of EHF patients decreased,CD8+T cell and double CD4+CD8+ cell(double positive cells,DP cell) counts of EHF patients increased obviously,and 25 cases of EHF in recovery stage returned to normal.And in comparison with HIV,CMV and EBV patients,DP cell counts of EHF patients increased obviously.CONCLUSIONS T lymphocytes of EHF decrease obviously but could be resumed,detection of amounts of lymphocyte subsets and CD4+CD8+ cells can provide an early diagnosis method to EHF.
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AIM:To detect the treatment of K562 leukemia cells with bortezomib altering the expression of genes fas,bcl-2,bcl2l12,bim,bax,caspase-9 and caspase-3.METHODS:MTT assay was used to detect the inhibition of proliferation.Apoptosis was detected by Annexin-V staining and mitochondrial transmembrane potential(??m).RT-PCR was used to analyze the mRNA expressions of fas,bcl-2,bcl2l12,bim,bax,caspase-3 and caspase-9.RESULTS:Bortezomib caused a time-and dose-dependent inhibition of cell proliferation and IC50 of 24 h and 48 h were 161.41 nmol/L and 96.33 nmol/L,respectively.At the concentration of 104 nmol/L,bortezomib induced apoptosis in a time-dependent manner,including increasing annexin-V positivity and decreasing the ??m.RT-PCR showed that bortezomib up-regulated the mRNA expression of fas,bcl2l12,caspase-9 and caspase-3,but mRNA expressions of bcl-2,bim and bax did not changed obviously.CONCLUSION:Bortezomib inhibits the proliferation of K562 and induces apoptosis,in which fas,bcl2l12,caspase-9 or caspase-3 gene is one of the main genes taking part in.