Foryst-Ludwig Anna, Neumann Manfred, Schneider-Brachert Wulf, Naumann Michael
Institute of Experimental Internal Medicine, Otto-von-Guericke-University, Leipziger Str. 44, Magdeburg 39120, Germany.
Biochem Biophys Res Commun. 2004 Apr 16;316(4):1065-72. doi: 10.1016/j.bbrc.2004.02.158.
Infection of epithelial cells by the microbial pathogen Helicobacter pylori leads to activation of the transcription factor nuclear factor kappaB (NF-kappaB), the induction of pro-inflammatory cytokine/chemokine genes, and the motogenic response (cell scattering). Here we report that H. pylori-induced NF-kappaB activation and the subsequent release of interleukin 8 (IL-8) are inhibited by curcumin (diferuloylmethane), a yellow pigment in turmeric (Curcuma longa L.). Our results demonstrate that curcumin inhibits IkappaBalpha degradation, the activity of IkappaB kinases alpha and beta (IKKalpha and beta), and NF-kappaB DNA-binding. The mitogen-activated protein kinases (MAPK), extracellular signal-regulated kinases 1/2 (ERK1/2) and p38, which are also activated by H. pylori infection, were not inhibited by curcumin. Further, the H. pylori-induced motogenic response was blocked by curcumin. We conclude that curcumin, due to inhibition of NF-kappaB activation and cell scattering, should be considered as a potential therapeutic agent effective against pathogenic processes initiated by H. pylori infection.
微生物病原体幽门螺杆菌感染上皮细胞会导致转录因子核因子κB（NF-κB）激活、促炎细胞因子/趋化因子基因的诱导以及促运动反应（细胞分散）。在此我们报告，姜黄素（二阿魏酰甲烷），一种姜黄（Curcuma longa L.）中的黄色色素，可抑制幽门螺杆菌诱导的NF-κB激活以及随后白细胞介素8（IL-8）的释放。我们的结果表明，姜黄素抑制IκBα降解、IκB激酶α和β（IKKα和β）的活性以及NF-κB与DNA的结合。同样被幽门螺杆菌感染激活的丝裂原活化蛋白激酶（MAPK）、细胞外信号调节激酶1/2（ERK1/2）和p38，不受姜黄素抑制。此外，姜黄素阻断了幽门螺杆菌诱导的促运动反应。我们得出结论，由于姜黄素抑制NF-κB激活和细胞分散，应被视为一种对幽门螺杆菌感染引发的致病过程有效的潜在治疗剂。
