桥本甲状腺炎患者外周血单个核细胞程序性死亡因子5的表达及其意义

Expression of PDCD5 in Peripheral Blood Monocytes of Patients with Hashimoto's Thyroiditis

目的探讨程序性死亡因子5(PDCD5)在桥本甲状腺炎(HT)患者外周血单个核细胞(PBMC)中的表达及其与HT发生发展之间的关系。方法选取华北煤炭医学院附属医院2006年3—8月内分泌门诊或住院HT患者60例(HT组)及同期体检健康者40例(对照组)。并根据HT患者血清抗甲状腺微粒体抗体(TMAb)水平,将HT组患者分为HT1组(TMAb≤45%)36例和HT2组(TMAb>45%)24例。采用半定量逆转录聚合酶链反应(RT-PCR)方法测定HT组和对照组受检者PBMC PDCD5 mRNA的表达水平,然后比较HT1组和HT2组患者甲状腺功能、血清甲状腺球蛋白抗体(TGAb)水平及PBMC PDCD5 mRNA表达水平。结果 (1)HT组患者PBMC PDCD5mRNA表达阳性率及相对表达水平均高于对照组〔86.7%(52/60)与60.0%(24/40),(0.87±0.19)与(0.38±0.08)〕,差异有统计学意义(χ2=9.355,t=4.870,P均<0.01)。(2)HT2组患者血清TGAb水平及PBMC PDCD5mRNA表达水平均高于HT1组〔(75.1±18.9)%与(50.4±10.7)%,(1.02±0.08)与(0.60±0.12)〕,差异有统计学意义(t值分别为6.400和15.041,P均<0.01)。结论 HT患者PBMC PDCD5 mRNA的表达上调,且随病情加重PDCD5表达增加,提示PDCD5可能通过增加其表达量而导致异常的淋巴细胞凋亡,从而参与HT的发生和发展。

Objective To explore the expression of programmed cell death 5（PDCD5） in peripheral blood monocytes（PBMC） of patients with Hashimoto＇s thyroiditis（HT） and to investigate their relationship.Methods 60 HT patients（HT group） admitted to Affiliated Hospital of North China Coal Medical University from March to August in 2006 and 40 healthy people（control group） at the same time were involved into the study.The HT patients were further divided into HT1 group（TMAb≤ 45%,36 cases） and HT2 group（TMAb 45%,24 cases）.RT-PCR method was used to the expression of PBMC PDCD5 mRNA in HT group and control group.The function of thyroid,TGAb levels and expression of PBMC PDCD5 mRNA were compared between the HT2 group and HT2 group.Results（1） The positive expression rate and expression level of PBMC PDCD5 mRNA in HT group were both significantly higher than the control group 〔86.7%（52 /60） vs.60.0%（24 /40）,（0.87 ± 0.19） vs.（0.38 ± 0.08） 〕（χ2 = 9.355,t = 4.870,P both 0.01）.（2） The TGAb level and PBMC PDCD5 mRNA expression level were both significantly higher in HT2 group compared with HT1 group 〔（75.1 ± 18.9） % vs.（50.4 ± 10.7） %,（1.02 ± 0.08） vs.（0.60 ± 0.12） 〕（t = 6.400,15.041,P both 0.01）.Conclusion The up-regulation of expression of PBMC PDCD5 mRNA in HT patients and the aggravation of HT suggests that abnormal apoptosis of lymphocytes led by the overexpression of PDCD5 plays an important role in the pathogenesis of HT.