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This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin II (AngII) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngII. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngII model group, cells were treated with AngII at 10(-7) mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngII+astilbin groups, cells were treated with AngII (at 10(-7) mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabolism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G(0)/G(1) phase were increased and that of G(2)/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngII could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngII-mediated proliferation of RASMCs by blocking the transition of RASMCs from G(0)/G(1) phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.
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Objective To explore the effects of CD40Ig gene transfer in vitro on cardiac allograft survival in mice. Methods The recombinant adenovirus vector carrying murine CD40 extracellular domain and human IgG Fc fusion gene (AdCD40Ig) was constructed. Using BALB/c mice as donors and C57BL/6 mice as recipients, the model of mice abdomen heterotopical heart transplantation was set up. In the experimental group, the isolated donor heart was transfected with AdCD40Ig, then transplanted to recipient. The other groups included empty vector transfected control group, untransfected control group, and syngeneic control group (the donors and the recipients were C57BL/6 mice). The survival time of donor hearts and the infiltration of inflammatory cells in heart allograft were observed. The expression of CD40Ig fusion protein in recipient was identified by Sandwich ELISA; The IFN-? producing cells in recipient was determined by FACS. Results The survival time of the cardiac allograft in experimental group was ( 15.8? 0.7) days, significantly longer than empty vector transfected control group and untransfected control group (P
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AIM:To investigate the effect of ovarian carcinoma cells on ? chain expression and the secretion of Tc1/Tc2 type cytokine in CD8+ T cells,and its role in the ovarian carcinoma induced immunosuppression.METHODS:The supernatants of human ovarian carcinoma cell lines of OVCAR3,CAOV3 and SKOV3 and RPMI-1640 were added into CD8+ T cells(groups I,II,III,and control),which were isolated from the peripheral venous blood of healthy persons.The expression of ? chain was analyzed by Western blotting.Thiazolyl blue(MTT)method was used to detect the effects of those cell line supernatants on the growth of CD8+ T cells.The secretion of the Tc1 type cytokine interferon(IFN)-? mRNA and the Tc2 type cytokine interferon(IL)-10 mRNA were detected by RT-PCR.RESULTS:The expression of ? chain was significantly lower in groups I,II,and III in comparison with that in control group.The absorbance at the wavelength 570 nm of CD8+ T cells culture in the group I,II,and III was all significantly lower than that in the control group.The IFN-? expression was significantly lower in groups I,II,and III in comparison with that in control group,while the expression of IL-10 was significantly higher.CONCLUSION:Ovarian carcinoma may suppress CD8+ T cell proliferation and secretion of the Tc1/Tc2 type cytokine through inhibition of ? chain,which may play an important role in the ovarian carcinoma induced immunosuppression.
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0.05).Conclusion:MBL B allele is not a risk component in the developing process of SLE Chinese patients.