【摘要】 目的探讨蛋白激酶C(PKC)对ITP患儿T细胞核因子-кB(NF-кB)活化的调控作用。方法分别从35例特发性血小板减少性紫癜(ITP)患儿及30例健康儿童的外周血中分离出T细胞并分成3组培养,即空白对照组,加入PKC的激活剂PMA的PMA组,同时加入PKC激活剂PMA与抑制剂H-7的PMA+H-7组,分别用免疫组化法和Westernblot检测NF-кB和抑制蛋白кB(I-кB)。结果ITP患儿的PMA组NF-кB活化的细胞百分比显著高于空白对照组和正常儿童的PMA组(P<0.05),且I-кB水平显著低于上述两组(P<0.05),而ITP的PMA+H-7组NF-кB活化的细胞百分比显著低于ITP的PMA组,且I-кB水平显著高于该组(P<0.05)。结论ITP患儿T细胞NF-кB的活化可能受PKC信号传导的调控,T淋巴细胞PKC-NF-кB信号传导途径的激活可能是ITP的发病机制之一。更多还原

【Abstract】 Objectives To explore the role of protein kinase C (PKC) in regulating the activation of nuclear factor-кB (NF- кB) in T lymphocyte from idiopathic thrombocytopenic purpura (ITP) children. Methods Peripheral blood from ITP children (n = 35) and healthy children (n = 30) were collected. T lymphocytes were purified and divided into three groups separately: control group,phorbol 12- myristate 13- acetate (PMA) treated group,and PMA + H-7 treated group. The expression of NF- кB and inhibitor protein- кB (I- кB) was detected by immunohistochemical staining and Western blot,respectively. Results The percentage of cells with active NF- кB was significantly higher and the expression level of I- кB was significantly lower in ITP-PMA group than that in ITP- control group and healthy- PMA group respectively (all P < 0.05). The percentage of cells with active NF- кB was significantly lower and the expression level of I- кB was significantly higher in ITP -PMA + H-7 group than that in ITP-PMA group(both P < 0.05). Conclusions It revealed that the activation of NF- кB in ITP T lymphocyte may be regulated by PKC, and the activation of PKC- NF- кB signal pathway of T Lymphocyte may play an important role in the pathogenesis of ITP.更多还原