Bülbül Neşe, Pala Elif, İğci Yusuf Ziya, Göğebakan Bülent, Öztuzcu Serdar, Cengiz Beyhan, Bayraktar Recep, Dağ Muhammet Sait, Aydınlı Musa
Department of Internal Medicine, Nizip State Hospital, Gaziantep, Turkey.
Turk J Gastroenterol. 2014 Dec;25(6):634-8. doi: 10.5152/tjg.2014.5926.
BACKGROUND/AIMS: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which catalyzes the formation of reactive oxygen species (ROS) in phagocytic cells, has five subunits: p67phox ("phox"refers to "phagocyte oxidase"), p47phox, p40phox, p22phox, and gp91phox (catalytic subunit). Oxidative stress resulting from the accumulation of ROS and/or defective removal of ROS by antioxidants has detrimental effects on cellular functions and may contribute to chronic inflammation. Disruption of the colonic mucosa due to the dysregulation of antioxidants or transformation enzymes may play a role in the pathogenesis of ulcerative colitis (UC) and influence the clinical features of this disease. In this study, we examined the expression of the gene encoding NADPH oxidase subunit p22phox cytochrome b-245, alphapolypeptidein the colonic mucosa to test its possible contribution in the pathogenesis of UC.
Expression levels of mRNA in the inflamed and non-inflamed colonic mucosa (determined using colonoscopy)of 22 patients with UC and in the normal mucosa of 22 healthy controls were analyzed using real-time polymerase chain reaction.
Expression levels of mRNA were not significantly different between patients with inflamed and non-inflamed colonic mucosa (p>0.05) and betweenpatients with inflamed colonicmucosa and healthy controls (p>0.05).
Although our data suggest that expression of the gene encoding p22phox is not associated with chronic inflammation in patients with UC, other mechanisms can affect oxidative stress in these patients.
背景/目的:烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶可催化吞噬细胞中活性氧(ROS)的形成,它有五个亚基:p67phox(“phox”指“吞噬细胞氧化酶”)、p47phox、p40phox、p22phox和gp91phox(催化亚基)。ROS积累和/或抗氧化剂对ROS清除缺陷导致的氧化应激会对细胞功能产生有害影响,并可能导致慢性炎症。抗氧化剂或转化酶失调引起的结肠黏膜破坏可能在溃疡性结肠炎(UC)的发病机制中起作用,并影响该疾病的临床特征。在本研究中,我们检测了结肠黏膜中编码NADPH氧化酶亚基p22phox细胞色素b - 245α多肽的基因表达,以测试其在UC发病机制中的可能作用。
使用实时聚合酶链反应分析22例UC患者炎症和非炎症结肠黏膜(通过结肠镜检查确定)以及22例健康对照者正常黏膜中的mRNA表达水平。
炎症和非炎症结肠黏膜患者之间(p>0.05)以及炎症结肠黏膜患者与健康对照者之间(p>0.05)的mRNA表达水平无显著差异。
虽然我们的数据表明编码p22phox的基因表达与UC患者的慢性炎症无关,但其他机制可能影响这些患者的氧化应激。