CAJ | 학술논문

目的通过检测系统性红斑狼疮（SLE）模型鼠脾脏树突状细胞（DC）中雌激素受体（ER）的表达及对体外雌激素的反应性是否异常，探索雌激素调控DC参与SLE发病的机制。方法红细胞裂解法收集SLE模型鼠---NZB/wF1雌鼠及BALB/c雌鼠的脾脏单个核细胞，抗小鼠CD11 c单抗标记磁珠纯化DC，以无酚红RPMI-1640及葡聚糖-活性炭处理的新生牛血清体外培养 DC，加入不同浓度10-8 mol/L，10-7 mol/L，10-6 mol/L的雌二醇（E2）体外处理24 h，RT-PCR检测DC胞内ER的mRNA水平。结果两种小鼠脾DC均表达ERα，但不表达ERβ；NZB/wF1雌鼠脾DC的ERα基础表达显著高于同周龄的BALB/c雌鼠（0 mol/L组P＜0.05）；低浓度10-8 mol/L E2显著增加两种鼠脾DC的ERα表达（NZB/wF1鼠P＜0.05， BALB/c鼠P＜0.05），中浓度10-7 mol/L （ NZB/wF1鼠P＜0.05， BALB/c鼠P＜0.05）和高浓度10-6 mol/L （NZB/wF1鼠P＜0.05，BALB/c鼠P＜0.05）E2显著降低两种鼠脾DC的ERα表达。结论 ER表达在狼疮鼠中存在明显异常，不同剂量雌激素对其受体调控作用不同，提示雌激素可能通过调控DC的ER参与SLE发病。
목적통과검측계통성홍반랑창（SLE）모형서비장수돌상세포（DC）중자격소수체（ER）적표체급대체외자격소적반응성시부이상，탐색자격소조공DC삼여SLE발병적궤제。방법홍세포렬해법수집SLE모형서---NZB/wF1자서급BALB/c자서적비장단개핵세포，항소서CD11 c단항표기자주순화DC，이무분홍RPMI-1640급포취당-활성탄처리적신생우혈청체외배양 DC，가입불동농도10-8 mol/L，10-7 mol/L，10-6 mol/L적자이순（E2）체외처리24 h，RT-PCR검측DC포내ER적mRNA수평。결과량충소서비DC균표체ERα，단불표체ERβ；NZB/wF1자서비DC적ERα기출표체현저고우동주령적BALB/c자서（0 mol/L조P＜0.05）；저농도10-8 mol/L E2현저증가량충서비DC적ERα표체（NZB/wF1서P＜0.05， BALB/c서P＜0.05），중농도10-7 mol/L （ NZB/wF1서P＜0.05， BALB/c서P＜0.05）화고농도10-6 mol/L （NZB/wF1서P＜0.05，BALB/c서P＜0.05）E2현저강저량충서비DC적ERα표체。결론 ER표체재랑창서중존재명현이상，불동제량자격소대기수체조공작용불동，제시자격소가능통과조공DC적ER삼여SLE발병。
Objective To research the mechanism how estrogen abnormally modulates dendritic cells ( DC) to involve in systemic lupus erythematosus(SLE)by investigating the expression of estrogen receptor (ER)in spleen DCs of SLE model mice and the reaction of ER to estrogen in vitro.Methods Harvest the spleen mononuclear cells of female NZB/wF1 and BALB/c mice by lysing erythrocytes.Monoclonal anti-mouse CD11c antibody-labeled bead was used to purify DCs from mononuclear cells .DC were cultured in phenol red-free RPMI1640 with 10%charcoal-dextran treated fetal bovine serum and different concentration:10 -8 mol/L,10 -7 mol/L,10 -6 mol/L of 17β-estrodiol (E2)for 24 hours.RT-PCR was used to detect the mRNA level of ER in E2-stimulated lymphocytes.Results The spleen DC of female NZB/wF1 and BALB/c mice both express the mRNA of ERα,but not ERβ.The expression of ERαin NZB/wF1 spleen DC was significantly higher than same week-old BALB/c mice ( 0 mol/L P<0.05 ) .Low (10 -8 mol/L) concentration of E2 obviously promoted the expression of ERαin the two kinds of mice ( NZB/wF1 mice P<0.05,BALB/c mice P<0.05).Middle(10 -7 mol/L,NZB/wF1 mice P<0.05,BALB/c mice P<0.05) and high ( 10 -6 mol/L, NZB/wF1 mice P <0.05 , BALB/c mice P <0.05 ) concentration of E2 decreased the expression of ERα.Conclusion The expression of estrogen receptor is obviously abnormal in lupus model mice .ER reactions to various concentration of estrogen in vitro are different .It suggests that estrogen may involve in the pathogenesis of SLE by modulating estrogen receptors in DC .