Objective To evaluate the effects of tacrolimus on the secretion of IL-6 and sIL-2R as well as the expression of IL-6 and sIL-2R mRNA by lymphocytes.Methods Jurkat human lymphoma cells were cultured and treated with tacrolimus of different concentrations.Enzyme linked immunosorbent assay was performed to determine the levels of IL-6 and sIL-2R in the supernatant of Jurkat cells at 48 hours after treatment with tacrolimus of 0,10,102,103 and 104 nmol/L,and real time reverse transcription PCR to measure the expression of IL-6 mRNA and sIL-2R mRNA of Jurkat cells at 48 hours after treatment with tacrolimus of 102 nmol/L.Results Tacrolimus of 102 - 104 nmol/L could suppress the secretion of IL-6 and sIL-2R from Jurkat cells (all P＜ 0.05),with a more marked suppressing effect achieved by the use of tacrolimus at 103 - 104 nmol/L.The expressions of IL-6 and sIL-2R mRNA from Jurkat cells were downregulated by tacrolimus of 102 nmol/L (both P ＜ 0.05).Conclusion Tacrolimus at certain concentrations could downregulate the secretion of IL-6 and sIL-2R as well as the expression of IL-6 and sIL-2R mRNA by lymphocytes.

Objective To evaluate the effect of intrathecal ganglioside GM-1 on chronic central pain (CCP) following spinal cord injury in rats.Methods Thirty-two adult male Sprague-Dawley rats,weighing 220-250 g,in which intrathecal catheters were successfully implanted,were randomly divided into 4 groups (n =8 each) using a random number table:control group (group C); group CCP; normal saline group (group N) and ganglioside GM-1 group (group GM).CCP was induced according to modified Allen method in CCP,N and GM groups.In group GM,ganglioside GM-1 20 mg/kg was injected intrathecally once a day,for 5 consecutive days,starting from 14th day after CCP,while the equal volume of nomal saline 10 μl was injected intrathecally in group N.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 4,8,16,24 and 48 h after the end of administration.The rats were then sacrificedat at 7 d after the end of adminmistration and L1 segment of the spinal cord was removed for determination of the expression of NMDA receptor 1 (NR1) by immuno-histochemistry.Results Compared with group C,MWT and TWL were significantly decreased,and NR1 expression was up-regulated in CCP and N groups (P ＜ 0.01),and no significant changes were found in MWT,TWL and NR1 expression in group GM (P ＞ 0.05).Compared with group CCP,no significant changes were found in MWT,TWL and NR1 expression in group N (P ＞ 0.05),and MWT and TWL were significantly increased,and NR1 expression was down-regulated in group GM (P ＜ 0.05).Conclusion Ganglioside GM-1 can alleviate CCP following spinal cord injury in rats and inhibition of expression of NR1 in the spinal cord may be involved in the mechanism.

Objective To evaluate the effects of ischemic postconditioning (IPO) on c-fos protein expression during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-five adult male Sprague-Dawley rats,aged 8-12 weeks,weighing 200-250 g,were randomly allocated into 3 groups (n =25 each) using a random number table:sham operation group (group S),I/R group and IPO group.Renal I/R injury was induced by clamping the bilateral renal pedicles for 1 h followed by 24 h of reperfusion in I/R and IPO groups.Five animals were sacrificed at 1,3,6,12 and 24 h of reperfusion and the left kidneys were removed for microscopic examination and for determination of the expression of c-fos protein by immunohistochemistry.Results Compared with S group,the expression of c-fos protein was significantly up-regulated at each time point during reperfusion in I/R and IPO groups.Compared with I/R group,the expression of c-fos protein was significantly down-regulated at each time point during reperfusion in group IPO.The pathologic changes were significantly attenuated in group IPO as compared with group I/R.Conclusion The mechanism by which IPO attenuates renal I/R injury is related to down-regulation of c-fos protein expression in the renal tissues of rats.

Objective To evaluate the role of C-type lectin domain family 2,member B (CLEC2B) gene in the pathogenesis of vitiligo.Methods Real time fluorescence-based PCR was performed to detect the expression of CLEC2B mRNA in the peripheral blood and lesional skin of 37 patients with vitiligo as well as in the peripheral blood and normal skin of 40 healthy controls.Data were statistically analyzed by t test and chisquare test.Results Among the 37 patients,23 had progressive vitiligo,14 stable vitiligo,31 vitiligo vulgaris,6 segmental vitiligo.The expression level of CLEC2B mRNA was significantly higher in vitiligo lesions than in the control skin (1.21 ± 0.03 vs.1.00,t =4.432,P ＜ 0.05),but was of no significant difference in peripheral blood between the patients and healthy controls (1.02 ± 0.05 vs.1.00,t =1.435,P ＞ 0.05).Increased expression of CLEC2B mRNA was noted in lesions of vulgaris vitiligo compared with those of segmental vitiligo (1.21 ± 0.03 vs.1.02 ± 0.01,t =5.330,P ＜ 0.05),as well as in lesions of progressive vitiligo compared with those of stable vitiligo (1.25 ± 0.05 vs.1.08 ± 0.03,t =3.046,P ＜ 0.05).No significant difference was observed in the expression of CLEC2B mRNA among lesions of vitiligo with different courses (P ＞ 0.05).Conclusion The differential expression of CLEC2B mRNA may take part in the pathogenesis of vitiligo.