Objective To evaluate the serum histamine-releasing activity of patients with chronic urticaria and explore the pathogenesis of chronic urticaria. Methods Sixty-two chronic urticaria patients were studied by using in vivo autologous serum skin test (ASST) and in vitro histamine release assay of human cutaneous mast cells incubated with the patient′s sera. Results Twenty-four out of 62 patients showed a wheal response to autologous serum (38.71%). Sera from patients with chronic urticaria released a significantly higher quantity of histamine compared with the control subjects (P

In order to investigate the effects of cis-UCA on cell -mediated immunity, we established a murine model of DTH response to DNP6OVA which is indicated by the increasing in the ear thickness of the mouse after resensitization, compared with those of the mouse injected with 200 g cis - UCA and trans -UCA intraperitoneally (i. p. ). The average of the increasing in ear thickness of each group was 9. 1 1. 13 10-2 mm (n=8, the number of ears) for the group administrated with cis-UCA; 17. 45 0. 88 10 - 2 mm (n= 8) for the group administrated with trans-UCA ; 16. 43 + 1. 83 10 - 2 mm(n= 7) for control group. It is suggested that there are immunosuppression of DTH response to DNP6OVA in mouse administrated with ets-UCA and no effecs of trans-UCA on this response.

0.05).ASST+ patients had larger wheals(P

Objective To study the effects of the IL-1 receptor antagonist (IL-1Ra) on matrix metalloproteinase 1 (MMP-1) expression in UV-irradiated fibroblasts. Methods Simulating the impact of environmental ultraviolet (UV) light on human skin, UVA-irradiated human fibroblasts were cultured in medium obtained from UVB-irradiated HaCaT cells. MMP-1 was detected by ELISA in the culture medium of fibroblasts. After treatment with IL-1Ra, the mRNA expression levels of C-Jun, C-Fos and GAPDH (internal control) of fibroblasts were measured by real-time fluorescent quantitative RT-PCR. Results Production of MMP-1 by UVA (10 J/cm2)-irradiated fibroblasts was increased in culture medium from UVB-irradiated HaCaT cells. The fibroblasts produced significantly higher levels of MMP-1 in culture medium from HaCaT cells treated without UVB than those with 15 mJ/cm2 UVB (t = 8.413,P= 0.014). However, IL-1Ra inhibited MMP-1 production of fibroblasts in a dose-dependent manner. Standard curves of real-time fluorescent quantitative RT-PCR showed a linear correlation between the copy number and the threshold cycle (Tc). Melting curves confirmed the specificity of PCR products. The original copy numbers of C-Jun and C-Fos as well as the ratios of the numbers to the GAPDH copy number showed that IL-1Ra inhibited the C-Jun mRNA expression of fibroblasts in a dose-dependent manner but had no significant effects on C-Fos mRNA expression. Conclusions The culture medium from UVB-irradiated HaCaT cells can promote MMP-1 production by UVA-irradiated fibroblasts. IL-1Ra reduces MMP-1 production via inhibition of C-Jun mRNA expression.

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis-urocanic acid. Method The auto lymphocyte proliferation test with Langerhans＇ cell (LC) in guinea -pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10. 5%, the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4% or 50%, respectively. The lymphocyte proliferation was almost completely suppressed by200J/m2 UVB radiation, while the inhibition of LC function by cis-urocanic acid was weak. Conclusion UVB significantly inhibits LC auto -stimulation in dose -dependent way, which may play an important role in UVB induced immunosuppression.

Objective To establish a cell line with repressed expression of p53 by transfecting a plasmid construct expressing short hairpin RNA(shRNA)targeting p53 into human skin fibroblasts(HSFs),and to evaluate the effect of repression of p53 expression on the senescence in HSFs.Methods The eukaryotic expressing plasmid pGCsi-p53 containing shRNA targeting p53 gene was transfected into HSFs with lipofectamine.Subsequently,the cells were selected by G418,and resistant cell clones were chosen and expanded.Reverse transcription-PCR and real time fluorescence-based quanitative PCR were performed to determine the expression of p53 gene,and Western blot to detect the expression of p53 protein in HSFs.The senescence in HSFs was evaluated by SA β-gal staining,and cell proliferation by methyl thiazolyl tetrazolium(MTT)assay.Results A HSF clone with repressed expression of p53 was established successfully.The expressions of p53 mRNA and protein were downregulated in transfected HSFs compared with untransfected HSFs(0.09 ± 0.03 vs.0.32 ± 0.04,0.11 ± 0.04 vs.0.84 ± 0.05,both P ＜ 0.01).The percentage of senescent cells was 13.47％ ± 1.01％ in the transfected HSFs,significantly lower than that in untransfected HSFs(18.10％ ± 0.66％,P ＜ 0.05).As MTT assay showed,the proliferation was accelerated in transfected HSFs compared with untransfected HSFs(P ＜ 0.05).Conclusions The repression of p53 expression decelerates the senescence in HSFs,but promotes the proliferation of HSFs.

Cao reported that melagenine extracted from human placenta was effective in the clinical treatment of vitiligo, to elucidate the possible mechanism involved, melagenine and placenta peptide were added to melanocytes in the culture, and the culture without melagenine as control. The results obtained by MTT showed that melagenine can stimulate melanoeyte proliferation, its promoting rate was 42.5%, while placenta peptide got a promoting rate of 5.9%, the difference was significant (P

Objective To study the immunosuppression mechanism induced by ultraviolet (UV) and cis urocanic acid. Method The auto lymphocyte proliferation test with Langerhans′ cell (LC) in guinea-pig was performed. Results In exposure to low dose of UVB (25 J/m2) radiation, the inhibition rate of lymphocyte proliferation stimulated by LC was 10.5％ , the inhibition rates of UVB radiation in doses of 50 J/m2 and 100 J/m2 were 22.4％ or 50％ , respectively. The lymphocyte proliferation was almost completely suppressed by 200 J/m2 UVB radiation, while the inhibition of LC function by cis urocanic acid was weak. Conclusion UVB significantly inhibits LC auto-stimulation in dose-dependent way, which may play an important role in UVB induced immunosuppression.

0.25)levels in the two groups.In the group treated with42mJ/cm 2 UVB irradiation followed by the addition of EGCG,the numbers of apoptotic and dead cells and Fas mRNA were decreased,but bcl-2protein was increased.Conclusions Low dosage of UVB irradiation could induce apoptosis of keratinocytes.High dosage of UVB irradiation might result in cell death.EGCG could reduce UVB-induced apoptosis of keratinocytes by increasing bcl-2protein and decreasing Fas mRNA.

Objective To explore the effects of antisense NF-?B p65 oligodeoxynucleotides on UV-induced IL-6 secretion of keratinocytes. Methods NF-?B p65 oligodeoxynucleotides were transfected to a keratinocyte cell line, HaCaT cells, mediated by lipofectamine. The NF-?B p65 protein in the cells was measured by Western blot assay, the mRNA level of NF-?B p65 was detected by RT-PCR, and UV-induced IL-6 level was determined by ELISA pre- and post-transfection and/or UVB irradiation. Results The NF-?B p65 protein expression was significantly increased in UVB (10, 20, 30 mJ/cm2 ) irradiation groups as compared with that of the control groups (P