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Expression of nicotinamide adenine dinucleotide phosphate oxidase in chronic rhinosinusitis with nasal polyps

烟酰胺腺嘌呤二核苷酸磷酸 医学 鼻息肉 慢性鼻-鼻窦炎 烟酰胺腺嘌呤二核苷酸 氧化酶试验 鼻窦炎 磷酸盐 内科学 生物化学 外科 NAD+激酶 化学
作者
Kaili Zheng,Jin Hao,Lei Xiao,Min Wang,Yan Zhao,Dachuan Fan,Ying Li,Xiangdong Wang,Luo Zhang
出处
期刊:International Forum of Allergy & Rhinology [Wiley]
卷期号:10 (5): 646-655 被引量:18
标识
DOI:10.1002/alr.22530
摘要

Background Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase produces reactive oxygen species (ROS) involved in oxidative stress and signal transduction. Recent studies have suggested that NADPH oxidase is associated with the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). The aim of this study was to detect the expression of NADPH oxidase subunits and 4‐hydroxynonenal (4‐HNE) in nasal polyp tissue and normal nasal mucosa, in order to explore the possible role played by NADPH oxidase in the pathogenesis of CRSwNP. Methods Thirteen patients with CRSwNP and 9 normal control subjects were selected to participate in this study, in which we evaluated the expression of different NADPH oxidase subunits (gp91phox, p67phox, p47phox, and p22phox) in nasal polyp (NP) tissue and control mucosa by Western blotting and real‐time polymerase chain reaction (PCR). Immunohistochemistry and immunofluorescence staining were used to detect expression of the p67phox subunit and 4‐HNE in NP tissue and normal nasal mucosa. Results Western blot and real‐time PCR results showed that p67phox expression was significantly increased in NP tissue when compared with its expression in control mucosa (p = 0.004). p67phox was expressed in the eosinophils and neutrophils found in NP tissue, but not in the macrophages. Additionally, the levels of 4‐HNE expression were also significantly increased in NP tissue when compared with control mucosa (p = 0.001). Conclusion The levels of p67phox messenger RNA (mRNA) and protein as well as 4‐HNE were both upregulated in NP tissue, suggesting that p67phox and oxidative stress play roles in the pathogenesis of CRSwNP.
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