Purpose:Our study is to find out the inhibitory action of recombinant human TNF-related apoptosis-inducing ligand(TRAIL) on ovarian cancer cell line cultured in vitro. Methods:MTT was applied to assay the inhibiting action of various concentration of TRAIL on two ovarian cancer cell lines of 3AO and HO-8910.The apoptosis rates were measured by flow cytometry. Results:The growth of human ovarian cancer cells was effectively inhibited by TRAIL. A clear dose- and time-dependent correlation between TRAIL concentration and the degree of apoptosis induction was observed with up to 43.20% apoptotic cells after 24 h of incubation with 50 ng/ml TRAIL. The cells assumed typical cell apoptosis configuration. Conclusions:TRAIL can effectively inhibit the growth of ovarian cancer cells and induce apoptosis of the cells.

To investigate the pathogenic mechanism of interleukin 6(IL-6) in the tubulointerstitial lesions of patients with active lupus nephritis(LN). Methods Uninary IL-6 from 42 active LN cases and the renal tissues sections from 15 of them were examined by performing ELISA and in situ hybridization with IL-6 cDNA probe labelled by digoxingenin respectively. Results In 36/42 (85.7%) of active LN patients, uninary IL-6 content was higher than or equal to 5 pg/mg ,cr, while no one case did in normal controls. Uninary IL-6 content was highly correlated with the uninary ft-m and NAG excretion respectively. In normal tubules and interstitium, IL-6 mRNA was undetectable. For all sections from 15 active cases, IL-6 mRNA was found in tubular and interstitial cells, and the distribution correlated with the extent of tubulointerstitial lesions. Conclusion IL-6 is probably involved in tubulointerstitial lesions of patients with active lupus nephritis.

Objective To explore derivation of renocortieal prostaglandins in C-BSA nephritis. Methods The interfering effect of goat-antiplatelet IgG serum(APS)on this model was studied. Results The levels of renocortical PGE_2、6-keto-PGF_(1?) (PGI_2)、TXA_2 were all reduced in experimental group. The pathological damage of experimental group were less severe in comparison with the model group. Proteinuria of the experimental group was alleviated. Conclusion Platelet may play a pathogenetic role of C-BSA nephritis and renocortical prostaglandins partly derive from platelets.

Objective To investigate the effects of IFN-? and IL-4 on MIP- ? production of peripheral blood mononuclear cells (PBMC) in lupus nephritis (LN) Methods MIP-1? expression in supematants was determined by Elisa and MLP-l? mRNA in PBMC was detected by RT-PCR. Results (1) IFN-? increased MIP-1? prouduction of PBMC in LN. (2) IL-4 inhibited MIP-1? production of PBMC in LN. (3) No significant effect on PBMC in controls was found by either IFN-? or IL-4. Conclusion IFN-? enhances MLP- 1? production of PBMC in LN wherease LL-4 inhibits it.

Aim To investigate whether there is IL-12 signaling pathway through lck/P38/c-jun in splenic cells obtained from lupus mouse and its effect on splenic cells. Methods Mice with graft versus host disease were used as lupus nephritis model. Activity of Lck tyrosine kinase, p38 phosphorylation and mRNA expression of c-jun in splenic cells were determined by autoradiography, Western blot and Northern blot, respectively. Results There were higher levels of Lck activity, p38 phosphorylation and c-jun expression of IL-12-stimulated splenic cells from lupus model when compared with that observed in similarly treated splenic cells from normal control. The Lck activity and p38 phosphorylation were almost inhibited by Lck inhibitor PP1, on the other hand, p35 specific inhibitor SB203580 decreased phosphorylation of p38. In addition, expression of c-Jun was also inhibited by PP1 or SB203580 although splenic cells were stimulated with IL-12. Conclusion Aberrant murine splenic cell, IL-12-me-diated intracelluar signaling pathway through lck/p38/c-Jun were involved in immunologic damage.

To observe the role of parathyroid hormone PTH( 1 - 84) and platelet cytosolic free calcium I pt[ Ca2 + ] i in regulation of blood pressure on hemodialysis (HD) patients. Methods Fura-2 fluorometry and immunoradioassy werw used to detect PTH(1 - 84) and pttCa2+ ]i in 24 HD patients. Results The resting pt[Ca?+ ]i and PTH(1 - 84) increased in HD cases, and they were significantly higher in uremic patients with hypertension than ones without hypertension. The resting pt[Ca2+ ]i was correlated to PTH( 1 - 84) in HD cases. The multivariate stepwise regression analysis showed the PTH( 1 - 84) and pt[Ca2 + ]i are probably mains factors to affect the blood pressure in HD cases. Conclusion PTH(l - 84) and pt[Ca2+ ji are main factors affecting the blood pressure in uremic patients.

Objective:To investigate chemokine RANTES(Regulated upon Activation.Normal T cell Expressed and Secreted)expression in the chronic graft versus host disease(GVHD) murine lupus nephritis model and effect of the recipe of LangChuangFang on it.Methods:A microwave based immunohistochemistry(SP) and RT PCR were used to detect the expression of RANTES in the kidney of model,therapeutic group and normal control.At the same time,the correlation between expression of RANTES and renal injures in model was examined.Results:LangChuangFang protected renal function,which was coincided with amelioration of pathologic lesions especially tubulointersitial injury.This was associated with the amelioration of RANTES protein and mRNA expression in model.Conclusion:RANTES involved in the process of renal injury in vivo,LangChuangFang can treat lupus as immunosuppressive agent by decreasing RANTES production.

Objective:To detect MIP 1? mRNA in kidney specimens in lupus nephritis(LN) patients and investigate its association with clinical and pathological features.Methods:MIP 1? mRNA were identified by in situ hybridization.Results:MIP 1? mRNA were detected in gromeluli,cortical tubular cells and interstitum of LN specimens wherase no MIP 1? mRNA was found in normal specimens.There were especially obvious MIP 1? expression in IV type LN specimens.MIP 1? expression in LN gromeruli,tubular cells and interstitium were correlated positively with LN histological activity index.Conclusion:There were enhancement of MIP 1? mRNA expression in LN kidney specimens,especially in IV type LN.MIP 1? expression in LN specimens were related with active inflammatory injury of glomeruli and tubulointerstitium.

AIM:To observe the expression of chemokine fractalkine,and its receptor,CX3CR1,in kidneys of lupus-prone BXSB mice,and their changes after treatment with prednisone. The role of fractalkine and CX3CR1 in the pathogenesis of lupus nephritis was also discussed. METHODS:Twelve 12-week-old male BXSB mice were randomly divided into two groups,the prednisone treatment group (BXSB-prednisone group,n=6) and the experimental control group (BXSB group,n=6). Six male C57BL/6J mice at the same weeks of age served as a normal control group (C57BL/6J group). Both the C57BL/6J and the BXSB group of mice received a daily intragastric administration of 0.5 mL normal saline. The BXSB-prednisone group of mice was given a daily intragastric administration of prednisone (0.18 mg/20 g BW) dissolved in 0.5 mL normal saline. All treatments lasted for 10 weeks. The mRNA and protein expressions of fractalkine and CX3CR1 in kidneys of mice were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis respectively. The changes of laboratory index and the kidney histopathology of mice were also investigated. RESULTS:The mRNA and protein expressions of fractalkine and CX3CR1 in kidneys of BXSB mice were significantly higher than those in C57BL/6J mice. The expressions of fractalkine and CX3CR1 in BXSB-prednisone group of mice were much lower than those in BXSB group of mice,accompanied by the lower serum IgG,IgM and anti-dsDNA antibody levels as well as blood urea nitrogen,serum creatinine and urine protein. The glomerular immune complex deposition and the kidney histopathology were also significantly improved in BXSB-prednisone group of mice. CONCLUSION:These results indicate that fractalkine and CX3CR1 participate in the pathogenesis of lupus nephritis in BXSB mice,and the effect of glucocorticoids treatment may be attributed,in part,to its ability to inhibit the expression of fractalkine in kidney.

Objective:To investigate the effect of anti-CD134 mAb or CTLA4Ig on ConA induced splenic cell proliferation,Th cytokine secretion and production of anti-dsDNA antibody from splenic lymphtocyte in vitro in lupus-prone BXSB mice. Methods:Eighteen male lupus-prone BXSB mice model and 6 syngeneic normal C57BL/6 male mice were used in the experiment. The model mice were divided into three groups:un-treated group,Lupus recipe(LR) treated group and prednisone(pred. ) treated group. The mice's splenic cell suspension from above groups was culture stimulated by ConA respectively. The splenic cells from un-treated model mice were further divided into Anti-GD134L mAb,CTLA4Ig or Anti-CD134L mAb + CTLA4Ig treated subgroups. The ConA induced splenic cell proliferation was measured by MTT colorimetric assay. The levels of IFN-?, IL-6 and anti-dsDNA antibody in cell supernatant were measured by ELISA. Results; (1 )The splenic cell proliferative reaction and contents of IFN-?,IL-6 and anti-dsDNA antibody in cell supernatant of either spontaneous or ConA induced culture in the un-treated model group were obviously higher than that of the normal control or other groups. (2) The splenic cell proliferative reaction and production of IFN-?,IL-6 and anti-dsDNA antibody in the CD134L/CTLA4Ig treated group,LR treated goup or pred. treated group was not different from the normal control significantly. (3)To compared with CD134L treated group or CTLA4Ig treated gruop,the CD134L/CTLA4Ig and prednisone reduced significantly the splenic cell proliferative reaction and production of IFN-?,IL-6 and anti-dsDNA antibody in cell supernatant of either spontaneous or ConA induced culture,while no difference was found between CD134L treated group and CTLA4Ig treated proup. Conclusion:The lupus-prone BXSB mice might present abnormal lymphocyte proliferation,spontaneously express cytokines and secrete high level of autoantibody during the SLE development. LR and corticosteroids could obviously inhibit the abnormal lymphocyte proliferation;reduce the Th cytokine formation and antoantibody production Blockade of CD134-CD134L or B7-CD28 costimulatory pathway by Anti-CD134L rnAb or CT-LA4Ig could inhibit the activation of T cells and B cells like LR and corticosteroids. Furthermore, by blockade of both CD134-CD134L and CD28-B7 pathways,the frequency of alloreactive T cell was markedly reduced and was maintained at low levels so as to treat SLE effectively.