Objective To detect anti-cell membrane DNA ( cmDNA) antibody with human B lym-phocyte Raji cells and human promyelocytic leukemia HL60 cells as substrates and to compare the diagnostic value of anti-cmDNA antibody with that of anti-nucleosome antibody ( AnuA ) , anti-Sm antibody and anti-double-stranded DNA ( dsDNA) antibody in juvenile systemic lupus erythematosus ( JSLE) patients. Meth-ods We recruited 92 JSLE patients and 71 patients with other rheumatic diseases. Anti-cmDNA antibody an-dantinuclear antibody ( ANA ) was detected in patient serum by indirect immunofluorescence assays ( IIF ) . Anti-dsDNA antibody were detected by combining enzyme-linked immuno sorbent assay ( ELISA) and IIF. Anti-Sm antibody were detected by double immunodiffusion assay and immunoblotting, while anti-nucleosome antibody ( AnuA) were detected by ELISA. We collected concurrent clinical data. Results Anti-cmDNA antibody demonstrated stronger intensity of fluorescent patterns in using Raji cells as substrate than HL60 cells. JSLE patients had a significantly higher positive percentage of anti-cmDNA than patients with other rheu-matoid diseases. The sensitivity of anti-cmDNA on cell line Raji was higher than that of anti-dsDNA and anti-Sm (P<0. 01), the specificity of anti-cmDNA was close to anti-dsDNA (P>0. 05) and was lower than anti-Sm and AnuA (P<0. 01). The sensitivity of anti-cmDNA was similar to AnuA (P>0. 05) and the specificity was lower than AnuA (P<0. 01). The sensitivities of anti-dsDNA, anti-Sm and AnuA by combining with an-ti-cmDNA were much higher than that of the above antibody detected respectively ( P<0. 05 ) . Anti-cmDNA had no correlation with SLE disease activity index ( P=0. 907 ) . Conclusion The high sensitivity and speci-ficity of anti-cmDNA antibody make it a valuable diagnostic tool for JSLE. Combined detection of anti-cmDNA and other autoantibody might further improve the sensitivity in JSLE. Anti-cmDNA detected with IIF on cell line Raji was better than cell line HL60.

Objective:To observe any effect of photodynamic therapy (PDT) mediated by curcumin (CUR) on the proliferation of vascular smooth muscle cells (VSMCs) induced by platelet-derived growth factor-BB (PDGF-BB) through the phosphatidylinositol 3-kinase (PI3k)/serine threonine protein kinase (AKT) signaling pathway and explore its possible mechanism.Methods:Twenty μg/L of PDGF-BB was used to induce proliferation of VSMCs in A7R5 rat aortic smooth muscle cells and mouse aortic smooth muscle cells. Well-cultured VSMCs were randomly divided into a normal group, a PDGF-BB group, a curcumin group, and a low-dose PDT group (irradiated for 60s), a medium-dose PDT group (irradiated for 120s), and a high-dose PDT group (irradiated for 180s). The normal group was not given any intervention, and the PDGF-BB group was starved overnight and then stimulated for 24h by adding fresh medium containing 20μg/L of PDGF-BB. The curcumin group was first given the same intervention as the PDGF-BB group, and then placed in a medium containing 20μmol/L of curcumin for 6h. The PDT groups were first given the same intervention as the curcumin group, and then irradiated using a 425nm laser after removal of the medium. A CCK8 cell counting kit was used to detect the survival rate of VSMCs in the PDT groups after irradiation with the different laser doses. VSMC proliferation was detected using 5-ethynyl-2′-deoxyuridine (EDU) positive labeling. The cell cycle was observed using flow cytometry, and the expression levels of related phosphorylated proteins of the PI3K/AKT pathway and proliferating cell nuclear antigen were detected using western blotting.Results:The CCK-8 counts suggested that 120s was the optimum irradiation dose. The cell survival rates in the medium-dose and high-dose PDT groups were significantly different from the PDGF-BB group′s average. The proportion of proliferating cells in the PDT groups was significantly lower than in the PDGF-BB group. The proportion of cells in the G0 or G1 phase was significantly lower in the PDT group than in the normal group, while that in the G2 or M phase was significantly higher than in the normal and PDGF-BB groups. The expression of proliferating cell nuclear antigen and the phosphorylated proteins of the PI3K/AKT pathway had decreased significantly in the PDT group compared with the PDGF-BB group.Conclusion:CUR-mediated PDT inhibits PDGF-BB-induced proliferation of vascular smooth muscle cells, probably by down-regulating the expression of phosphorylated proteins related to the PI3K/AKT pathway.