宫颈病变组织中PKR与NF-κBp65的表达与磷酸化观察

Expression and Phosphorylation of PKR and NF-κB p65 in Cervical Lesions

目的 探讨宫颈病变组织内蛋白激酶R（PKR）、核因子（NF）-κB p65的表达及磷酸化的意义，高危型人乳头状瘤病毒（hsHPV）对两者表达及磷酸化的影响，以及三者的关系。方法 以67例宫颈癌、149例宫颈上皮内瘤样病变（CINⅠ-Ⅲ）、15例正常人宫颈组织为观察对象。检测各组hsHPV阳性表达情况，采用免疫组化SP法检测组织内PKR、磷酸化型PKR（p-PKR）、NF-κB p65和磷酸化型NF-κB p65（p-NF-κB p65）在上述分组中的表达。结果231例中hsHPV阳性136例，阴性95例。胞浆中PKR、p-PKR在hsHPV阳性组的表达低于hsHPV阴性组（27.2%和11.0% vs 41.1%和21.1%，χ2分别为4.858、4.371，均P＜0.05），在胞浆和胞核中NF-κB p65、p-NF-κB p65在hsHPV阳性组的表达高于hsHPV阴性组（46.3%、25.7%、22.8%和12.5% vs 32.6%、14.7%、11.6%和24.2%，χ2分别为4.345、4.048、4.729、4.650，均P＜0.05）；在胞浆和胞核中NF-κB p65（＋）组PKR的阳性表达率低于NF-κBp65（-）组（25.5%比38.0%和20.4% vs 36.3%，χ2分别为3.898、4.396，P＜0.05），p-NF-κB p65（＋）组在胞浆中PKR的阳性表达率低于p-NF-κBp65（-）组（19.0% vs 36.0%，χ2=4.462，P＜0.05）。结论hsHPV可能抑制PKR的表达及磷酸化而促进NF-κBp65的表达及磷酸化，NF-κBp65的表达及磷酸化对PKR的表达可能有抑制作用；三者间的调节作用可能与宫颈癌的发生发展有关。

Objective To identify the significance of expression and phosphorylation of protein kinase R（PKR） and nuclear factor NF-κB p65 in cervical lesions, and the effect of high-risk human papilloma virus （hsHPV） on expression and phosphorylation of R（PKR） and NF-κB p65. Methods A total of 67 patients with cervical cancer, 149 patients with cervi- cal intraepithelial neoplasia （CIN I - m） and 15 normal control were included in this study. The expression levels of PKR, phosphorylated PKR （p-PKR）, NF-κB p65 and phosphorylated NF-κB p65 （p-NF-κB p65） were detected by immunohisto- chemical SP method in three groups. Results The positive expression rates of PKR and p-PKR in cytoplasm were signifi- cantly lower in hsHPV positive group than those in hsHPV negative group （27.2% and 11.0% vs 41.1% and 21.1%, X2 = 4.858 and 4.371, P 〈 0.05）. The positive expression rates of NF-κB p65 and p-NF-κB p65 in cytoplasm and nucleus were significantly higher in hsHPV positive group than those in hsHPV negative group （46.3%, 25.7%, 22.8% and 12.5% vs 32.6%, 14.7%, 11.6% and 4.2% ,X2 = 4.345,4.048,4.729 and 4.650 respectively, P 〈 0.05）. The positive expression rates of PKR in kytoplasm and karyon were significantly lower in NF-κB p65 （＋） group than those in NF-κB p65 （-） group （25.5% vs 38.0% and 20.4% vs 36.3%,X2 = 3.898 and 4.396 respectively, P 〈 0.05）. The positive expression rate of PKR in kyto- plasm was significantly lower in p-NF-κB p65 （＋） group than those in p-NF-κB p65 （-） group （19.0% vs 36.0%, X2=4.462, P 〈 0.05）. Conclusion hsHPV may inhibit the expression and phosphory.tation of PKR but promote the expression and phosphorylation of NF-κB p65. The expression and phosphorylation of NF-κB p65 may inhibit the expression of PKR. Regu- lating effects of three may be associated with the generation and progression of cervical cancer.