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Objective To investigate the changes and clinical significance of the frequency of circulating CD4+ CD25+ regulatory T cells (Treg) in nonalcoholic fatty liver (NAFL) patients.Methods CD4+ CD25+ Treg in the peripheral blood from 50 NAFL patients and 50 healthy subjects were quantitatively analyzed using flow cytometry. Group t test or Mann-Whitney U test and Spearman's rank correlation test were used for statistical analysis.Results The proportion of circulating CD4+CD25+ Treg in NAFL patients was (5.39 ± 1.94)％,which was significantly higher than that in healthy controls [(4.21±1.52)％](t=3.385,P＜0.01).Further analysis revealed that the frequency of Treg was positively correlated with triglyceride (TG) level and body mass index (r=0.307 and 0.251,respectively; P=0.002 and 0.012,respectively),and negatively correlated with high density lipoproteincholesterol (HDL-C) (r=-0.306,P=0.002).Meanwhile,Treg in patients with high body mass index,high TG,low HDL-C,hypertension and metabolic syndrome (MS) were all higher than those in controls (t=2.294,2.533,3.154,2.010 and 4.454,respectively; all P＜0.05).But there was no significant difference between patients with high fasting blood glucose and controls (U=1143.500,P=0.471).Conclusion The increased frequency of peripheral Treg in NAFL patients may have some relations with the imbalance of proinflammation and anti-inflammation in NAFL patients who coexisting with MS.
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Objective:To study the molecular mechanism for momordin in inducing apoptosis of multidrug-resistant human chronic leukemia K562/A02 cells. Methods:The growth inhibition value of K562/A02 cells was detected by CCK-8 method. Cell apoptosis was analyzed by Annexin Ⅴ flow cytometry (FCM) and cell morphological examination. FCM was also used in determining expression of P-glycoprotein, p53 protein, bcl-2 protein and caspase activity. Results:Momordin inhibited the proliferation of K562/A02 cells in a dose-dependent manner. It also induced cell apoptosis, reduced the expression of P-glycoprotein, p53 protein and bcl-2 protein, and increased caspase-3 and caspase-8 activity.Conclusion:Momordin reversed the inhibition of apoptosis in multidrug-resistant K562/A02 cells. The molecular mechanism may be related with down-regulation of expression of p53 protein, P-glycoprotein, and bcl-2 protein and up-regulation of caspase-3 and caspase-8 activities.
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Objective To evaluate the alteration of CD4+ regulatory T cells in peripheral blood from patients with ankylosing spondylitis(AS). Methods Seventy-eight AS patients and 50 healthy individuals were included in this study. The proportion of CD4+CD25+CD127lo/- T cell population in CD4+ T cells as well as that cytotoxic T lymphocytes(CTL) and NK cells in lymphocytes was evaluated by flow cytometry. Serum TGF-β and TNF-α were measured by ELISA. The inhibitory function of CD4+CD25+ regulatory T cells was measured by mixed lymphocyte culture. Results The population of CD4+CD25+CD127lo/- T cells in peripheral blood of AS patients accounted for (4.36±1.21)% of CD4+ T lymphocytes, which was significantly lower than that in healthy individuals (P<0.05). The CD4+CD25+CD127lo/- T cells population in AS patients was positively correlated with TGF-β level, but negatively with TNF-α. Compared with healthy individuals, the function of CD4+CD25+ regulatory T cells in the inhibition of alloreactive T cells was lower in AS patients, which was related to the decreased secretion of TGF-β. Conclusion The CD4+ regulatory T cells in peripheral blood of AS patients are significantly decreased and its function is defective, which leads to immune regulatory dysfunction in vivo. It may be one of immune pathogenesis mechanisms of AS.
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Objective To investigate the effects of arsenic trioxide(ATO) on anti-dsDNA antibody and lymphocyte subsets proliferation in splenic cells of MRL/lpr mice.Methods MRL/lpr mice were divided into three groups: ATO group(0.4 mg/kg?d,ip),sodium chloride(NS) group(0.25 mL,ip),and cyclophosphamide(CTX) group(50 mg/kg?qw,ip).The control group consisted of 12 syngeneic normal C57/BL mice,which were sub-divided into ATO group(0.4 mg/kg?d,ip) and NS group(0.25 mL,ip).After two-month treatment,all mice were killed and their bodies and spleens were weighed.Anti-dsDNA antibody in serum were detected by ELISA.The percentage of different cell subsets was checked through flow cytometry.Results(1)The spleen index、serumlevel of anti-dsDNA antibody and the percentages of CD19+、CD3+、CD3+CD4+ lymphocytes in ATO group were much lower than those in NS group of MRL/lpr mice(P0.05). Conclusion Arsenic trioxide can inhibit the activation of T and B lymphocytes,increase the percentage of NK cell and reduce the serum level of auto-antibody.And it was of no effect in the normal mice.
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AIM: To explore the change of the expression of cell adhesion molecule CD_ 54 and CD_ 44 in erythroleukemic K562 apoptosis cells induced by momordin from momordica charantia seeds and study the effects of cell adhesion molecule CD_ 54 and CD_ 44 on cell apoptosis induced by momordin. METHODS: After the treatment of K562 cells with appropriated concentration momordin, CCK-8 test was employed to determine K562 cells growth; flow cytometry FACScan (FITC-Annexin V staining) and electron microscopy were used to detect apoptosis; The expression of CD_ 54 and CD_ 44 were examined by flow cytometry FACScan (FITC-CD_ 54 and PE-CD_ 44 staining). RESULTS: CCK-8 test showed K562 cells growth was significant inhibited by momordin; the apoptosis was detected by cell morphology and flow cytometry FACScan (FITC-Annexin V) in K562 cells after treatment by appropriated concentration momordin. The expressions of CD_ 54 and CD_ 44 in momordin treated K562 cells were 18.62 % and 1.32 % respectively, and in negative momordin treated K562 cells were 0.25 % and 0.17 % respectively, and momordin could up-expresses the protein of CD_ 54 18.37 % and CD_ 44 1.15 %. CONCLUSION: Momordin can markedly induce the K562 cell to apoptosis. The up-expressions of CD_ 54 exist in the process of apoptosis induced by momordin. The change of cell adhesion molecule maybe one of the key factors in the mechanisms of apoptosis induced by momordin, and its mechanism maybe involve in adhesion-dependent apoptosis.
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0.01). The new caries did not occur in the test group. DMF index was higher in the controls than that in the tested subjects(P
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AIM:To investigate the target killing effect of T lymphocytes with chimeric CD20scFv gene on Daudi cells and the activation of T lymphocytes.METHODS:Two kinds of plasmids were transfected into retrovirus-packed PA317 cell lines.The supernatant was collected from successfully transfected PA317 culture and was used to infect peripheral blood T lymphocytes.After one-week screening with G418,the cells were used to kill Daudi and K562 cells.The positive rates of AnnexinⅤ in Daudi cells were measured at different times points respectively by flow cytometry.Meanwhile,the level of IL-2 and IFN-? were determined by ELISA.RESULTS:The Annexin V positive rate was significant higher in Daudi cells compared to control K562 cell lines at 24 h.No difference of AnnexinV in Daudi cells was observed in CD20 modification T lymphocyte groups.The secretions of IL-2 and IFN-? in CD20scFv-CD80-IgGFc-CD28-? gene modified T cells co-cultured with Daudi cells were dramatically higher than that in CD20scFv-IgGFc group at 72 h.CONCLUSION:① The two kinds of genetic modified specific T cells have no significant difference in inducing early apoptosis of Daudi cells.CD28-? can't affect Daudi cell early apoptosis at the CD20scFv target killing.② The increase in the secretions of IL-2 and IFN-? is more obvious in CD20scFv-IgGFc-CD28-? group,indicating that the self-activation takes place in CD3? and CD28 modified T cells without MHC restriction and then increases the activation and killing function of T cells.