ABSTRACT
Objective To study the changes of the T-lymphocyte subsets in patients with Guillain-Barré syndrome(GBS)before and after intravenous immunoglobulin treatment(IVIG),and to explore the possible mechanism of the IVIG curing GBS further.Methods Chose 31 cases of clinically confirmed GBS were enrolled and compared before and after the treatment.According to the effect of the therapy,31 cases of the total were sub-divided into effective and ineffective groups.Relative counting of peripheral blood T-lymphocyte subsets was preformed with flow cytometry.Results ①The percentage of CD8+ T and CD4+CD29+ T cell was significantly lower(CD8+T:28.77%±11.02% vs 31.84%±12.35%,CD4+CD29+T:56.71%±12.44% vs 62.40%±12.72%,t=2.995,3.919,P＜0.05)after therapy,while the rate of CD4+/CD8+T and the percentage of CD4+CD45RA+T cell increased notably(t=2.368,3.860,P＜0.05);but there was no notable difference in the percentage of CD3+T and CD4+T cell.②The percentage of CD8+T and CD4+CD29+ T cell was significantly lower(t=2.144,3.343,P＜0.05)after the treatment,while the rate of CD4+/CD8+T and the percentage of CD4+CD45RA+T cell increased notably(t=2.159,3.277,P＜0.05)in the good curative effect group,but there was no change in the bad curative effect group.③61.29%(19/31)of the patients significantly improved by IVIG,and there was no death case.Conclusions T-lymphocyte subsets change in a varing degree after IVIG treatment in acute GBS patients,which lays an immunological foundation for the further study of pathogenesis and mechanism of IVIG curing GBS;effective on GBS,IVIG can actively suppress pathogenetic condition and promote the recovery of nrevous function.
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Objective To investigate the expression of suppressor of cytokine signaling genes (SOCSs) and JAKs mRNA in the acute myloid leukemia(AML) patients. Methods The expression of SOCSs and JAKs mRNA as well as TYK2 in AML patients and healthy adults as normal contrals (NC) was measured with RT-PCR. Results The expression of SOCS 1,4,5 and 7 in AML patients was lower than those in normal control and AML with remis-sion (P<0.01),but the expression of SOCS 3 and 6 was higher than those in normal control and remission AML(P<0.01),however there was no significant difference in SOC2 between groups. The expressions of JAK2 ,JAK3 and TYK2 in AML were significantly higher than those in patients with remission and normal control(P<0.05). The ex-pression of JAK1 mRNA in relapsed AML was higher than that in normal control group(P<0.05),but the latter has no statistical significance between beginning treatment and normal group(P>0.05). Conclusion The deletion and degradion of SOCS 1,4,5 and 7 present in AML patients and JAKs expression is significantly increased, suggesting that both of them may co-participate in the pathogenesis of AML.
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AIM: To investigate the effects of ?-elemene,extracted from curcuma wenyujin,on proliferation, cell cycle and apoptosis of human multiple myeloma RPMI-8226 cells. METHODS: The effect of ?-elemene on the growth of human multiple myeloma RPMI-8226 cells was studied through MTT assay,cell cycle and apoptosis was studied by combined Annexin-V protein iodide staining,The morphological changes was studied by combining Hoechst33342-PI staining. RESULTS: ?-elemene inhibited the proliferation of RPMI-8226 cells in a time-and dose- dependent manner. Compared with the control cells,the proportions of the RPMI-8226 cells in the G0 /G1 phase rose,and the proportions of the RPMI-8226 cells in the S and G2 /M phases fell decreased. RPMI-8226 cells treated with ?-elemene for 48 h induced apoptosis in a dose-dependent manner. CONCLUSION: ?-elemene is able to inhibit the proliferation of RPMI-8226 cells by arresting the cell cycle and inducing the cell apoptosis.
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AIM: To investigate the role of mitochondrial ceramidase in mitochondrial functions, especially in the regulation of apoptosis. METHODS: pCDNA3.1/His-MtCDase plasmid, containing mitochondrial ceramidase cDNA sequence, was transfected into K562 cells by liposome, and G418 was used to screen the positive clones. A stable transfected K562 cell line was established and defined as ‘K562TC’. The differences between K562 and K562TC cells in serum withdrawal resistance and Bcl-2 protein expression were evaluated by annexin V/PI test, flow cytometry and Western blotting, respectively. RESULTS: K562TC cells with elevated Bcl-2 protein expression level identified by FCM or Western blotting showed stronger resistance to apoptosis induced by serum withdrawal than their parental cells. Inhibition of mitochondrial ceramidase expression in K562TC cells by its specific antisense oligodeoxynucleotide was correlated with a decrease in Bcl-2 protein level. N, N'-dimethylsphingosine (DMS), a sphingosine kinase inhibitor, depleted intracellular sphingosine-1-phosphate (SPP) production, also abrogated Bcl-2 protein expression in K562TC cells, while exogenous sphingosine-1-phosphate up-regulated Bcl-2 protein level in K562 cells. CONCLUSION: Mitochondrial ceramidase overexpression in K562 cells leads to markedly elevated level of Bcl-2 protein and results in more resistance to serum withdrawal. This effect is initiated not by sphingosine, the direct metabolite of mitochondrial ceramidase, but via sphingosine-1-phosphate, its phosphorylated form, indicating that mitochondrial ceramidase, through its sphingoid metabolite sphingosine-1-phosphate, up-regulates Bcl-2 protein expression in K562 cells.