Objective To observe the effects of a novel HLA-derived peptide, RDP1258, on the human peripheral blood mononuclear cell (PBMC) proliferation to ConA and MLR, and to investigate the mechanisms. Methods Peptide RDP1258 was chemically synthesized. The effects of the peptide on alloreactive cytotoxic activities of human PBMCs were observed using 3HTdR incorporation method. RDP1258, HLA-B2702.75-84, and control peptide were administrated respectively in every experiment. The activity of heme oxygenase-1 (HO-1) was analyzed by the enzymochemical method. Results The results showed that the synthetic HLA-derived peptide could obviously inhibit the proliferation of human PBMCs and inhibited HO activity in a dose-dependent manner in vitro. Conclusion HO-1 might participate in the inhibitory effect of RDP1258 on the proliferation of human PBMCs induced by mitogen and isoantigen.

Dendritic Cell Sarcoma, Interdigitating ; Humans ; Lymph Nodes ; Male ; Middle Aged

Objective To study the effect of chitosan-pCrmA nanoparticles on the apoptosis of chondrocytes induced by interleukin-1 beta (IL-1β).Methods Chitosan-pDNA nanoparticles were prepared and characterized.The transfection efficiency of chitosan-mediated pIRES2-EGFP was evaluated using fluorescence microscope.The cytotoxicity of chitosan-pIRES2-EGFP nanoparticles in primary rabbit chondrocytes was analyzed by MTT assay.The expression of chitosan-mediated pCrmA in primary rabbit chondrocytes was verified by Western blotting.The effect of chitosan-mediated CrmA on chondrocytes apoptosis induced by IL-1β were analyzed by TUNEL assay.One-way ANOVA was used to analysis.Results The size of chitosan-pDNA nanoparticles was 50 nm.The pDNA release of chitosan-pDNA nanoparticles appeared as biphasic release at pH 2.0 and pH 7.4 buffer.The expression of CrmA in rabbit primary chondrocytes mediated by chitosan could be detected.The chitosan-pIRES2-EGFP nanoparticles had no cytotoxicity.The apoptosis rate of chondrocytes in the chitosan-pCrmA nanoparticles treated group was significantly lower than that of the chitosan treated group (P＜0.05) and PBS group (P＜0.01).Conclsion Chitosan is an effective non-viral gene transfer vector.The CrmA mediated by chitosan can significantly inhibit chondrocytes apoptosis induced by IL-1β,suggesting that chitosan-pCrmA nanoparticles may be the treatment of osteoarthrifis.

Objective: To study the immunosuppression function of a novel HLA-derived pepride, RDP1258,and it' s mechanisms. Methods:A peptide derived from HLA,RDP1258,was chemically synthesized.The effects of the peptide on alloreactive cytotoxic activities of rat splenocytes were observed using 3H-TdR method.The heme oxygenase-1(HO-1) activity was analyzed by the enzyme chemistry method.Results:The results showed that the synthetic HLA-derived peptide can obviusly inhibit the proliferation of rat splenocytes and the peptide inhibited HO-1 activty in a dose-dependment manner in vitro.Conclusion:HO-1 might participate in the RDP1258 inhibiting the proliferation of rat splenocytes induced by mitogen and isoantigen.

Objective To observe the immunosuppression function of a novel HLA derived peptide, RDP1258, and to investigate the mechanisms. Methods The peptides derived from HLA, RDP1258, and HLA 2702.75 84 was synthesized chemically. The effects of the peptides on alloreactive cytotoxic activities of rat spleen cells were observed using 3H TdR incorporation method. The heme oxygenase 1 activity was detected by the enzyme chemistry method. Result The synthetic HLA derived peptides could obviously inhibit the proliferation of rat spleen cells and HO 1 activity in a dose dependent manner in vitro. Conclusion HO 1 may participate in the process of inhibitory effect of RDP1258 on the proliferation of rat spleen cells induced by mitogen or isoantigen.

Objective To investigate the immunosuppression function of a novel HLA derived peptide, RDP1258, and its mechanisms. Methods A peptide derived from HLA, RDP1258, was chemically synthesized by artificial solid phase synthesis. Effects of the peptide on alloreactive cytotoxic activity of rat spleen cells and heme oxygenase 1 (HO 1) activity were observed using 3H TdR method and enzyme chemistry method, respectively. Results The synthetic HLA derived peptide could obviously inhibit the proliferation of rat spleen cells and mixed lymphocyte reaction, and reduce HO activity in a dose dependent manner in vitro . Conclusion RDP1258 can significantly inhibit the proliferation of rat spleen cells induced by mitogen and isoantigen possibly by means of affecting HO 1 activity.

Animals ; Cell Line, Tumor ; Enoyl-CoA Hydratase ; genetics ; metabolism ; Liver Neoplasms, Experimental ; metabolism ; pathology ; Lymphatic Metastasis ; Mice ; Plasmids ; Recombinant Proteins ; genetics ; metabolism ; Transfection

The Wnt signaling pathway plays an important role in bone metabolism. Inducing the Wnt signaling pathway promotes bone formation while restraining it results in osteopenic states. Although the regulation of this signaling pathway may bring enormous therapeutic potential, it still requires cautious approach because of the risks of tumorigenesis. The role of the Wnt signaling pathway in bone metabolism and the molecular targets of therapeutic potential for osteoporosis are discussed in this review.

OBJECTIVETo evaluate the inhibitive effect of C-21 steroidal glycosides from the root of Cynanchum auriculatum (CGB) on rat glioma C6 cells.

METHODSC6 cells were treated with CGB for 24, 48,72 h at concentration of 30, 60, 120 mg/L, respectively. MTT assay was used for evaluating cell viability; fluorescence-activated cell sorting analysis after Annexin V/propidium iodide staining or single propidium iodide staining was used to test cell apoptosis and cell cycle.

RESULTSCGB at 30, 60, 120 mg/L concentration-dependently decreased C6 cell viability (P<0.001). CGB at 60 and 120 mg/L induced C6 cell apoptosis and cell cycle arrest. The fraction of G0/G1 cells was increased (P<0.05) and that of S phase cells was decreased (P<0.01).

CONCLUSIONCGB can inhibit the growth of rat glioma C6 cells, and induce apoptosis and G0/G1 cell cycle arrest.

Animals ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cynanchum ; chemistry ; Glioma ; pathology ; Monosaccharides ; pharmacology ; Rats ; Steroids ; pharmacology