广西医学
廣西醫學
엄서의학
GUANGXI MEDICAL JOURNAL
2015年
6期
758-760
,共3页
系统性红斑狼疮%激素抵抗%糖皮质激素受体%核质分布
繫統性紅斑狼瘡%激素牴抗%糖皮質激素受體%覈質分佈
계통성홍반랑창%격소저항%당피질격소수체%핵질분포
Systemic lupus erythematosus%Glucocorticoid resistance%Glucocorticoid receptor%Nucleoplasm distribution
目的:探讨激素抵抗型系统性红斑狼疮(SLE)患者外周血单核细胞(PBMC)中糖皮质激素受体α(GRα)表达的量及核质分布,推测 SLE 激素抵抗发生的可能机制。方法选取激素抵抗型 SLE 患者、激素敏感型 SLE 患者和健康对照各18例。 SLE 患者在完成治疗8周后,抽取所有对象外周血,分离单个核细胞,用 Western Blot 检测 GRα表达量,用免疫组化技术检测 GRα核质比。结果激素敏感组及激素抵抗组 PBMC 中 GRα表达明显低于健康对照组(P <0.05);激素抵抗组核质比低于敏感组及健康对照组(P <0.05)。结论GRα表达的下调及其核转运障碍可能在 SLE 患者糖皮质激素抵抗的发生中发挥关键作用。
目的:探討激素牴抗型繫統性紅斑狼瘡(SLE)患者外週血單覈細胞(PBMC)中糖皮質激素受體α(GRα)錶達的量及覈質分佈,推測 SLE 激素牴抗髮生的可能機製。方法選取激素牴抗型 SLE 患者、激素敏感型 SLE 患者和健康對照各18例。 SLE 患者在完成治療8週後,抽取所有對象外週血,分離單箇覈細胞,用 Western Blot 檢測 GRα錶達量,用免疫組化技術檢測 GRα覈質比。結果激素敏感組及激素牴抗組 PBMC 中 GRα錶達明顯低于健康對照組(P <0.05);激素牴抗組覈質比低于敏感組及健康對照組(P <0.05)。結論GRα錶達的下調及其覈轉運障礙可能在 SLE 患者糖皮質激素牴抗的髮生中髮揮關鍵作用。
목적:탐토격소저항형계통성홍반랑창(SLE)환자외주혈단핵세포(PBMC)중당피질격소수체α(GRα)표체적량급핵질분포,추측 SLE 격소저항발생적가능궤제。방법선취격소저항형 SLE 환자、격소민감형 SLE 환자화건강대조각18례。 SLE 환자재완성치료8주후,추취소유대상외주혈,분리단개핵세포,용 Western Blot 검측 GRα표체량,용면역조화기술검측 GRα핵질비。결과격소민감조급격소저항조 PBMC 중 GRα표체명현저우건강대조조(P <0.05);격소저항조핵질비저우민감조급건강대조조(P <0.05)。결론GRα표체적하조급기핵전운장애가능재 SLE 환자당피질격소저항적발생중발휘관건작용。
Objective To investigate the expression and nucleoplasm distribution of glucocorticoid receptor alpha(GRα) of peripheral blood mononuclear cell(PBMC) in patients with glucocorticoid-resistant systemic lupus erythematosus(SLE),aiming at conjecture the possible pathogenesis of glucocorticoid-resistant SLE.Methods Glucocorticoid-resistant SLE patients, glucocorticoid-sensitive SLE patients,and healthy controls,each of 18 cases,were selected.Eight weeks after the SLE patients had received the treatment,the peripheral blood of all subjects was extracted,and PBMC was isolated to determine the expression level of GRαby using Western Blot and GRαnucleocytoplasmic ratio by the immunohistochemistry technique.Results The glucocorticoid-resistant or glucocorticoid-sensitive SLE patients showed significantly lower expression level of GRαof PBMC compared with healthy controls(P <0.05),and the nucleocytoplasmic ratio in glucocorticoid-resistant SLE patients was lower than that in glucocorticoid-sensitive SLE patients or healthy controls(P <0.05). Conclusion The down-regulation of GRαexpression and nuclear transport barriers might play a key role in the activation of GC resistance among SLE patients.