Singh S, Aggarwal B B
Department of Molecular Oncology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
J Biol Chem. 1995 Oct 20;270(42):24995-5000. doi: 10.1074/jbc.270.42.24995.
When activated, NF-kappa B, a ubiquitous transcription factor, binds DNA as a heterodimeric complex composed of members of the Rel/NF-kappa B family of polypeptides. Because of its intimate involvement in host defense against disease, this transcription factor is an important target for therapeutic intervention. In the present report we demonstrate that curcumin (diferuloylmethane), a known anti-inflammatory and anticarcinogenic agent, is a potent inhibitor of NF-kappa B activation. Treatment of human myeloid ML-1a cells with tumor necrosis factor (TNF) rapidly activated NF-kappa B, which consists of p50 and p65 subunits, and this activation was inhibited by curcumin. AP-1 binding factors were also found to be down-modulated by curcumin, whereas the Sp1 binding factor was unaffected. Besides TNF, curcumin also blocked phorbol ester- and hydrogen peroxide-mediated activation of NF-kappa B. The TNF-dependent phosphorylation and degradation of I kappa B alpha was not observed in curcumin-treated cells; the translocation of p65 subunit to the nucleus was inhibited at the same time. The mechanism of action of curcumin was found to be different from that of protein tyrosine phosphatase inhibitors. Our results indicate that curcumin inhibits NF-kappa B activation pathway at a step before I kappa B alpha phosphorylation but after the convergence of various stimuli.
活化后,核因子-κB(NF-κB)作为一种普遍存在的转录因子,以由Rel/NF-κB多肽家族成员组成的异源二聚体复合物形式与DNA结合。由于其密切参与宿主对疾病的防御,这种转录因子是治疗干预的重要靶点。在本报告中,我们证明姜黄素(二阿魏酰甲烷),一种已知的抗炎和抗癌剂,是NF-κB活化的有效抑制剂。用肿瘤坏死因子(TNF)处理人髓样ML-1a细胞可迅速激活由p50和p65亚基组成的NF-κB,而这种激活被姜黄素抑制。AP-1结合因子也被发现受姜黄素下调,而Sp1结合因子未受影响。除TNF外,姜黄素还阻断佛波酯和过氧化氢介导的NF-κB活化。在经姜黄素处理的细胞中未观察到TNF依赖性的IκBα磷酸化和降解;同时p65亚基向细胞核的转位也受到抑制。发现姜黄素的作用机制不同于蛋白酪氨酸磷酸酶抑制剂。我们的结果表明,姜黄素在IκBα磷酸化之前但在各种刺激汇聚之后的步骤抑制NF-κB活化途径。