García-Trapero Jorge, Carceller Fernando, Dujovny Manuel, Cuevas Pedro
Departmento de Investigación, Hospital Universitario Ramón y Cajal, Universidad de Alcalá de Henares, E-28034-Madrid, Spain.
Neurol Res. 2004 Dec;26(8):816-24. doi: 10.1179/016164104X5110.
The nuclear transcription factor kappaB (NF-kappaB) is a cytoplasmic dimer that, as the family of mitogen-activated protein kinase (MAPK), can directly regulate the expression of early genes and genes involved in the stress response, following a variety of physiological or pathological stimuli. Both of them stimulate the transcription of many proteins, which are considered important during inflammation. A crucial role has been assigned to these factors in cellular proliferation and in neointimal hyperplasia secondary to the endothelial lesion of arterial vessels. On the other hand, it has been described that neomycin can have an inhibitory function on tumor cell proliferation, through the inhibition of different intracellular pathways of signaling, among them the NF-kappaB and MAPK pathways. Rat common carotid artery was subjected to balloon angioplasty. Neomycin sulfate (18 mg) was applied using pluronic acid gel on the adventitial surface of the injured vessel. MAPK and NF-kappaB activation was quantified after 24 hours with immunohistochemical staining. Neointimal formation was quantified after 14 days with morphometry. Immunohistochemistry results demonstrating MAPK and NF-kappaB activation reveal that both transcription factors are activated in the media of the control vessel wall. In contrast, the immunoreactivity for MAPK and NF-kappaB in the sections obtained from arteries treated with neomycin over 24 hours was insufficient or nonexistent. Treatment with neomycin on adventitia over 14 days in arteries on which angioplasty was performed shows a neointimal index (intimal area/medial area) decrease of 71% in comparison with arteries that were not treated. The adventitial neomycin treatment over 14 days produces a very significant increase (287.5%; p<0.0001) in the arterial luminal circumference in comparison with arteries treated with vehicle. These results support the theory that neomycin plays an important role against neointimal hyperplasia through the inhibition of MAPK and NF-kappaB activation.
核转录因子κB(NF-κB)是一种细胞质二聚体,与丝裂原活化蛋白激酶(MAPK)家族一样,在受到多种生理或病理刺激后,可直接调节早期基因以及参与应激反应的基因的表达。它们二者均能刺激许多蛋白质的转录,这些蛋白质在炎症过程中被认为是重要的。这些因子在细胞增殖以及继发于动脉血管内皮损伤后的新生内膜增生中发挥着关键作用。另一方面,已有研究表明,新霉素可通过抑制不同的细胞内信号传导途径,包括NF-κB和MAPK途径,对肿瘤细胞增殖产生抑制作用。对大鼠颈总动脉进行球囊血管成形术。将硫酸新霉素(18毫克)与普朗尼克酸凝胶一起应用于受损血管的外膜表面。24小时后通过免疫组织化学染色对MAPK和NF-κB的活化进行定量分析。14天后通过形态学测量对新生内膜形成进行定量分析。免疫组织化学结果显示MAPK和NF-κB的活化,表明这两种转录因子在对照血管壁的中膜中被激活。相比之下,在接受新霉素处理超过24小时的动脉切片中,MAPK和NF-κB的免疫反应性不足或不存在。在进行血管成形术的动脉外膜上用新霉素处理14天,与未处理的动脉相比,新生内膜指数(内膜面积/中膜面积)降低了71%。与用赋形剂处理的动脉相比,外膜新霉素处理14天可使动脉管腔周长显著增加(287.5%;p<0.0001)。这些结果支持了新霉素通过抑制MAPK和NF-κB活化对新生内膜增生起重要作用的理论。