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目的研究白介素１受体相关激酶２（ＩＲＡＫ－２）和磷脂酰肌醇 ３－激酶（ＰＩ ３－激酶）在白介素－１（ＩＬ－１）诱导核因子－κＢ（ＮＦ－κＢ）活化中的作用。方法 Ｌｉｐｏｆｅｃｔｉｏｎ介导反义ＩＲＡＫ－２寡核苷酸或反义ＰＩ３－激酶寡核苷酸转染ＨｅｐＧ２细胞后；用逆转录 ＰＣＲ法检测 ＩＲＡＫ－２ ｍＲＮＡ和ＰＩ３－激酶ｍＲＮＡ表达水平，以Ｓａｎｄｗｉｃｈ ＥＬＩＳＡ法检测ＮＦ－κＢ的活化。结果（１）反义ＩＲＡＫ－２寡核苷酸和反义ＰＩ３－激酶寡核苷酸分别抑制ＩＲＡＫ－２ ｍＲＮＡ和ＰＩ－３激酶ｍＲＮＡ的表达：（２）反义ＩＲＡＫ－２寡核苷酸或反义ＰＩ３－激酶寡核苷酸部分抑制ＮＦ－κＢ活化；（３）与反义ＩＲＡＫ－２寡核苷酸或反义ＰＩ ３－激酶寡核苷酸单独转染ＨｅｐＧ２细胞相比，反义ＩＲＡＫ－２寡核苷酸和反义ＰＩ ３－激酶寡核苷酸共转染ＨｅｐＧ２细胞对ＮＦ－ｋＢ的抑制作用明显增强。结论在ＨｅｐＧ２细胞中， ＩＲＡＫ－２和ＰＩ ３－激酶都调控 ＮＦ－κＢ活化但都不能完全激活 ＮＦ－κＢ，ＩＲＡＫ－２和 ＰＩ ３－激酶在调控 ＮＦ－κＢ活化时有协同作用。
Objective To investigate the effects of interleukin-1 receptor related kinase 2 (IRAK-2) and phosphatidylinositol 3-kinase (PI 3-kinase) on the activation of nuclear factor-κB induced by interleukin-1 effect. Methods Lipofection mediated the expression of IRAK-2 mRNA and PI3-kinase mRNA in HepG2 cells transfected with antisense IRAK-2 oligonucleotide or antisense PI3-kinase oligonucleotide. Sandwich ELISA Act test NF-κB activation. Results (1) Antisense IRAK-2 oligonucleotide and antisense PI3-kinase oligonucleotide inhibited the expression of IRAK-2 mRNA and PI-3 kinase mRNA, respectively: (2) antisense IRAK-2 oligonucleotide Or antisense PI3-kinase oligonucleotides partially inhibit NF-κB activation; (3) compared to the transfection of HepG2 cells with antisense IRAK-2 oligonucleotides or antisense PI 3-kinase oligonucleotides alone The inhibitory effect of IRAK-2 oligonucleotide and antisense PI 3-kinase oligonucleotide co-transfected HepG2 cells on NF-kB was significantly enhanced. Conclusion Both IRAK-2 and PI 3-kinase regulate the activation of NF-κB in HepG2 cells, but neither can activate NF-κB completely. Synergistic effect of IRAK-2 and PI 3-kinase on the regulation of NF-κB activation was observed.