目的探索可能影响不伴有继发性干燥综合征(sSS)的系统性红斑狼疮(SLE)患者发生干眼的细胞因子,并分析有关细胞因子的浓度与临床干眼指标之间的相关性。方法 54例诊断为SLE且符合纳入标准的患者被作为研究对象,根据患者的临床干眼指标分...目的探索可能影响不伴有继发性干燥综合征(sSS)的系统性红斑狼疮(SLE)患者发生干眼的细胞因子,并分析有关细胞因子的浓度与临床干眼指标之间的相关性。方法 54例诊断为SLE且符合纳入标准的患者被作为研究对象,根据患者的临床干眼指标分为干眼组( n =11)、干眼倾向组( n =25)、对照组( n =18)。用Western blot法检测各组患者血清中的基质金属蛋白酶2(MMP-2)及激肽释放酶13(Klk13)的含量,通过 ELISA法测量血清中的白介素1(IL-1)、 IL-6、肿瘤坏死因子α(TNF-α)的浓度。结果 MMP-2的蛋白相对表达量在干眼组与对照组之间的差异有统计学意义( P <0.05),IL-1的浓度在干眼倾向组明显高于对照组,差异有统计学意义( P <0.01),TNF-α的蛋白水平在干眼组与对照组之间的差异有统计学意义( P <0.05)。Klk13、IL-6的蛋白表达量在3组之间的差异无统计学意义( P >0.05)。结论 MMP-2、IL-1和TNF-α影响不伴有sSS的SLE患者的眼表情况,并且TNF-α可作为一个有效血清学指标反映眼表状况。展开更多
Objective:To observe the dynamic changes of interleukin--6(IL--6) and its effects on catabolism ofthe skeletal muscle protein in the early stage after scalding. Methods: After a model of Balb/C mice inflictedwith 18%-...Objective:To observe the dynamic changes of interleukin--6(IL--6) and its effects on catabolism ofthe skeletal muscle protein in the early stage after scalding. Methods: After a model of Balb/C mice inflictedwith 18%-- 20% TBSA full--thickness skin scald on the back and one hindleg was established, the proteincatabolic rate (TNR) and the level of 11.M6 in soleus muscle and serum were determined and the effects of IL6 on TNR of normal mice and those of 11.--6 antiserurn on TNR of the scalded mice wee observed during thefirst week after scalding. Results: The level of IL--6 was significantly increased and maintained during thefirst three days. TNR of the scalded leg was elevated to the peak on the 3rd day and then decreased graduallywhile that of the unscalded leg was increased only on the 2nd day after scalding. TNR was significantlyincreased when IL--6 was injected to the normal mice and IL--6 antiserum could significantly inhibit the. increased TNR of the scalded mice when it was injected intraperitoneally. Conclusion: The increase of IL--6 isrelated with local inflammatory response in the early stage after scalding and the high level of IL--6 canincrease the catabolic rate of muscle protein.展开更多
The reduced expression of miR-142-3p/5p in CD4^(+) T cells of SLE patients caused T cell hyperactivity and B cell hyperstimulation.This study aimed to investigate the mechanisms of regulating miR-142-3p/5p expression ...The reduced expression of miR-142-3p/5p in CD4^(+) T cells of SLE patients caused T cell hyperactivity and B cell hyperstimulation.This study aimed to investigate the mechanisms of regulating miR-142-3p/5p expression in SLE CD4^(+) T cells.The BCL-6 expression was significantly increased in SLE CD4^(+) T cells compared with normal controls,and the BCL-6 expression was inversely correlated with miR-142-3p/5p expression.BCL-6 suppresses the expression of miR-142-3p/5p by increasing H3K27me3 level and reducing H3K9/K14ac levels in SLE CD4^(+) T cells.BCL-6 regulates histone modifications in miR-142 promoter by recruiting EZH2 and HDAC5.Furthermore,we observed significantly decreased CD40L,ICOS,and IL-21 expression levels in SLE CD4^(+) T cells with BCL-6 interference,and obviously reduced autoantibody IgG production in autologous B cells co-cultured with BCL-6 inhibited SLE CD4^(+) T cells.Our study found that increased BCL-6 up-regulates H3K27me3 and down-regulates H3K9/14ac at miR-142 promoter in SLE CD4^(+) T cells.These factors induce a declination in miR-142-3p/5p expression,consequently resulting in CD4^(+) T cell hyperactivity.展开更多
文摘目的探索可能影响不伴有继发性干燥综合征(sSS)的系统性红斑狼疮(SLE)患者发生干眼的细胞因子,并分析有关细胞因子的浓度与临床干眼指标之间的相关性。方法 54例诊断为SLE且符合纳入标准的患者被作为研究对象,根据患者的临床干眼指标分为干眼组( n =11)、干眼倾向组( n =25)、对照组( n =18)。用Western blot法检测各组患者血清中的基质金属蛋白酶2(MMP-2)及激肽释放酶13(Klk13)的含量,通过 ELISA法测量血清中的白介素1(IL-1)、 IL-6、肿瘤坏死因子α(TNF-α)的浓度。结果 MMP-2的蛋白相对表达量在干眼组与对照组之间的差异有统计学意义( P <0.05),IL-1的浓度在干眼倾向组明显高于对照组,差异有统计学意义( P <0.01),TNF-α的蛋白水平在干眼组与对照组之间的差异有统计学意义( P <0.05)。Klk13、IL-6的蛋白表达量在3组之间的差异无统计学意义( P >0.05)。结论 MMP-2、IL-1和TNF-α影响不伴有sSS的SLE患者的眼表情况,并且TNF-α可作为一个有效血清学指标反映眼表状况。
文摘Objective:To observe the dynamic changes of interleukin--6(IL--6) and its effects on catabolism ofthe skeletal muscle protein in the early stage after scalding. Methods: After a model of Balb/C mice inflictedwith 18%-- 20% TBSA full--thickness skin scald on the back and one hindleg was established, the proteincatabolic rate (TNR) and the level of 11.M6 in soleus muscle and serum were determined and the effects of IL6 on TNR of normal mice and those of 11.--6 antiserurn on TNR of the scalded mice wee observed during thefirst week after scalding. Results: The level of IL--6 was significantly increased and maintained during thefirst three days. TNR of the scalded leg was elevated to the peak on the 3rd day and then decreased graduallywhile that of the unscalded leg was increased only on the 2nd day after scalding. TNR was significantlyincreased when IL--6 was injected to the normal mice and IL--6 antiserum could significantly inhibit the. increased TNR of the scalded mice when it was injected intraperitoneally. Conclusion: The increase of IL--6 isrelated with local inflammatory response in the early stage after scalding and the high level of IL--6 canincrease the catabolic rate of muscle protein.
基金by the National Natural Science Foundation of China(No.81402610 and No.81502733).
文摘The reduced expression of miR-142-3p/5p in CD4^(+) T cells of SLE patients caused T cell hyperactivity and B cell hyperstimulation.This study aimed to investigate the mechanisms of regulating miR-142-3p/5p expression in SLE CD4^(+) T cells.The BCL-6 expression was significantly increased in SLE CD4^(+) T cells compared with normal controls,and the BCL-6 expression was inversely correlated with miR-142-3p/5p expression.BCL-6 suppresses the expression of miR-142-3p/5p by increasing H3K27me3 level and reducing H3K9/K14ac levels in SLE CD4^(+) T cells.BCL-6 regulates histone modifications in miR-142 promoter by recruiting EZH2 and HDAC5.Furthermore,we observed significantly decreased CD40L,ICOS,and IL-21 expression levels in SLE CD4^(+) T cells with BCL-6 interference,and obviously reduced autoantibody IgG production in autologous B cells co-cultured with BCL-6 inhibited SLE CD4^(+) T cells.Our study found that increased BCL-6 up-regulates H3K27me3 and down-regulates H3K9/14ac at miR-142 promoter in SLE CD4^(+) T cells.These factors induce a declination in miR-142-3p/5p expression,consequently resulting in CD4^(+) T cell hyperactivity.
