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肝肾不足型重型斑秃患者血皮质醇及糖皮质激素受体mRNA的表达状况 被引量:6

Serum Cortisol and peripheral blood mononuclear cell glucocorticoid receptor mRNA expression in severe alopecia areata with liver-kidney deficiency syndrome
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摘要 目的探讨肝肾不足型重型斑秃患者血皮质醇、外周血单个核细胞(PBMC)中糖皮质激素受体mRNA(GRmRNA)表达状况与斑秃发病关系。方法采用化学发光法检测23例肝肾不足型重型斑秃患者血皮质醇表达水平,并用逆转录-实时荧光定量聚合酶链反应分别检测该23例患者应用糖皮质激素(GC)治疗前后PBMC中GRmRNA表达水平,并与20例正常对照组相对比。结果重型斑秃组与正常对照组两组血清皮质醇水平差异无统计学意义(P>0.05),重型斑秃组治疗前、后GRmRNA表达水平均低于正常对照组(P<0.05),并且治疗后GRmRNA表达水平比治疗前更低(P<0.01)。结论重型斑秃患者存在GC-GR紊乱,GRmRNA表达水平降低可能参与了重型斑秃的发病机制。肝肾不足型重型斑秃患者PBMC中GR mRNA表达水平显著低于正常对照组,这可能是重型斑秃肝肾不足证型在受体及基因水平上的病理变化,也可能是重型斑秃肝肾不足证型的微观本质之一。 Objective To investigate serum Cortisol level and glucocorticoid receptors(GR) mRNA expression in peripheral blood mononuclear cells(PBMCs) in patients with severe alopecia areata and liver-kidney deficiency syndrome and their involvement in the pathogenesis of severe alopecia areata.Methods In 32 patients with severe alopecia areata,serum Cortisol levels were measured by chemiluminescence assay and GR mRNA expression in the PBMCs was detected using reverse transcription real-time fluorescence quantitative PCR before and after treatment,with 20 normal subjects serving as the controls.Results Serum Cortisol level showed no significant difference between the cases and the normal controls(P〉0.05).The expression of GR mRNA in the PBMCs was significantly lower in the patients than in the normal controls(P〈0.05).The expression of GR mRNA was even lower after treatments in patients with alopecia areata(P〈0.01).Conclusion GC-GR disorder exists in severe alopecia areata.A decreased GR mRNA expression in the PBMCs can be involved in the pathogenesis of severe alopecia areata,and such pathological changes at the receptor and genetic levels might also serve as the microscopic basis of liver-kidbey deficiency syndrome in severe alopecia areata.
出处 《南方医科大学学报》 CAS CSCD 北大核心 2012年第2期230-233,共4页 Journal of Southern Medical University
基金 广东省中医药管理局科研课题(2050032)
关键词 重型斑秃 血皮质醇 糖皮质激素 受体 肝肾不足 severe alopecia areata serum Cortisol glucocorticoid receptors liver-kidney deficiency syndromes
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