Objective To investigate the possible role of high mobility group box 1 protein (HMGB1) and its advanced gly‐cation end products receptor (RAGE) in the pathogenesis of systemic lupus erythematosus (SLE) .Methods The enzyme‐linked immunosorbent assay (ELISA) was used to determine the level of plasma HMGB1 in 52 cases of SLE (SLE group) and 40 healthy females undergoing physical examination (HC group) ,at the same time real time quantitative polymerase chain reaction (RT‐qPCR) was employed to detect the expression of HMGB1 and RAGE mRNA in peripheral blood mononuclear cells (PBMCs) .The correlation between plasma HMGB1 ,PBMCs HMGB1 and RAGE mRNA levels with clinical indicators was analyzed .Results The levels of plasma HMGB1 ,PBMCs HMGB1 mRNA in the SLE group were significantly higher than those in the HC group ,the differences were statistically significant (P< 0 .05) ,while the level of PBMCs RAGE mRNA had no statistical difference (P>0 .05);the Spearman correlation analysis showed that the level of plasma HMGB1 was positively correlated with antinuclear anti‐bodies titers and SLEDAI score in the SLE patients (P<0 .01) ,while had no obvious correlation with the other clinical and labora‐tory indicators(P>0 .05);the HMGB1 mRNA expression level was positively correlated with the RAGE mRNA expression level and SLEDAI scores(P<0 .01 ,P<0 .05) ,and had no obvious correlation with other clinical and laboratory indicators (P>0 .05) . Conclusion The abnormal expression of plasma HMGB1 and PBMCs HMGB1 mRNA in SLE patients prompts that which might be involved in the occurrence and development of SLE ,might participate in the immune and inflammatory regulation of SLE .

Objective To investigate the role of high mobility group box 1 protein(HMGB1) and the receptor for advanced glycation end products (RAGE) in the pathogenesis of primary gouty arthritis (GA).Methods Enzyme-linked immunosorbent assay(ELISA) was used to determine the level of plasma HMGB1 in 68 acute gout (AG),48 quiescent gout (QG) and 45 healthy control(HC).Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to measure the expression of HMGB1 and RAGE mRNA in the peripheral blood mononuclear cells (PBMCs) in 68 AG,48 QG and 94 HC.One way ANOVA or Wilcoxon test and Spearman's correlations were used for statistical analysis.Results The level of plasma HMGB1,PBMCs HMGB1 and RAGE mRNA were significantly higher in GA than that in HC [(24±34) ng/ml,0.019±0.029,0.000 5±0.000 3] (P＜0.05),while the level of plasma HMGB1 and PBMCs HMGB1 mRNA were significantly higher in AG [(222±178) ng/ml,0.235±0.954,0.001 5±0.003 5] than that in QG [(107±176) ng/ml,0.044±0.117,0.001 3±0.000 9] (P＜0.05),and the level of PBMCs RAGE mRNA was higher in AG than that in QG (P＞0.05).In the GA patients,the level of plasma HMGB1 was positively correlated with white blood cell count,neutrophile granulocytes count,mononuclear cells and erythrocyte sedimentation rate (r=0.34,0.44,0.39,0.33; P＜0.05),while negatively correlated with apolipoprotein A1 (r=-0.28,P＜0.05); the level of PBMCs HMGB1 mRNA was positively correlated with RAGE mRNA,white blood cell counts,neutrophil counts,lymphocyte counts,serum total cholesterol level,low density lipoprotein level and apolipoprotein B100 level (r=0.29,0.36,0.26,0.28,0.29; P＜0.05),while negatively correlated with high density lipoprotein (r=-0.30,P＜0.01); the level of PBMCs RAGE mRNA was positively correlated with lymphocyte counts,total cholesterol and apolipoprotein B100 (r=0.35,0.35,0.44; P＜0.05).Conclusion HMGB1 and its signaling pathway may play important role in the pathogenesis of gouty arthritis,which may also be involved in the regulation of the lipid metabolism of gout.

Objective To investigate the mRNA and protein expression levels of telomeric-repeat binding factor-1 (TRF1) and TRF2 in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE),and the relations between these gene expression levels and clinical data of SLE patients were explored.Methods According to disease activity,these SLE patients were divided into the active group (40 cases) and the stable group (67 cases).These patients were also grouped as renal damage group (46 cases) and renal damage-free group (61 cases) based on their renal conditions.Healthy individuals (41 cases) were also included as control.Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to study the mRNA expression of TRF1 and TRF2.The protein levels of TRF1 and TRF2 were measured by Western Blot (WB).Independent-Samples t test or one-way analysis of variance (ANOVA) in conjunction with the Least-Significant Difference method (LSD method) wasperformed if the data were in normal distributions;otherwise,the Kruskal-Wallis test was applied.Spearman's correlation analysis was also used for statistical analysis.Results The mRNA and protein expression levels of TRF1 and TRF2 in the PBMCs of the active group (TRF1:0.003 1±0.003 3;TRF2:0.010 5±0.064 8) and renal damage group (TRF1:0.002 3 ±0.002 6;TRF2:0.004 3 ±0.003 3) were significantly increased compared to the stable group (TRF1:0.001 2±0.001 1;TRF2:0.004 2±0.008 6),the renal damage-free group (TRF1:0.001 3±0.001 8;TRF2:0.003 4±0.007 2) and healthy (TRF1:0.001 2±0.003 0;TRF2:0.003 4±0.002 7) individuals respectively (P＜0.05).In SLE patients,the expression levels of TRF1 mRNA were correlated with erythrocyte sedimentation rate (r=0.365,P＜0.05);the expression levels of TRF2 mRNA were correlated with SLEDAI score (r=0.270,P＜0.05),erythrocyte sedimentation rate (r=0.304,P＜0.05),creatinine (r=0.258,P＜0.05) and 24-hour urinary protein (r=0.344,P＜0.05).Conclusion Altered expression of TRF1 and TRF2 might be involved in the pathogenesis of Systemic lupus erythematosus.The positive correlation between TRF2 and SLEDAI score,24-hour urinary protein suggest that TRF2 might be usedas a biomarker for disease activity or renal damage in

Objective To investigate the role of long noncoding RNA-AK001903 in the pathogenesis of primary gout arthritis (GA).Methods The subjects were divided into four groups:30 acute gout patients (AGA),24 non-acute gout patients (NAGA),24 healthy controls and 24 hyperuricemia (HUA).Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to examine the expression of AK001903 in peripheral blood mononuclear cells (PBMCs) from four groups.100 μg/ml monosodium (MSU) was used to stimulate the peripheral blood of NAGA and healthy control patients.Then the expression of AK001903 was detected by RT-qPCR.Kruskal-Wallis test,Mann-Whitney test,Spearman correlations were used for statistical analysis.Results The expression level of AK001903 in the AGA group (0.079±0.022) and the NAGA group (0.071±0.021) were higher than the healthy control group (0.014±0.004).There was no significant difference between the NAGA group and the NAGA group (Z=-0.655,P＞0.05).Those of the GA group (0.078±0.018) and the HUA group(0.047±0.016) was higher than the healthy control group (0.014±0.004) (Z=-2.887,Z=-4.157;P＜0.05).Compared with the control group,the expression of AK001903 in NAGA and the healthy control group which were stimulated by MSU was significantly increased.The Spearman correlation analysis found that the AK001903 expression levels in the GA groups were correlated with TG (r=0.938,P＜0.05),VLDL (r=0.873,P＜0.05),GLU9 (r=0.671,P＜0.05) and were negatively correlated with apoA1 (r=-0.661,P＜0.05).Conclusion Altered expression of AK001903 may be involved in the process of imbalance between lipid metabolism and hyperuricemia,and takes part in the pathogenesis of GA.