Cheng Yuan-Kai, Hwang Guang-Yuh, Lin Chia-Der, Tsai Ming-Hsui, Tsai Shih-We, Chang Weng-Cheng
Department of Otolaryngology, China Medical University Hospital, Taichung, Taiwan.
Laryngoscope. 2006 Mar;116(3):417-22. doi: 10.1097/01.MLG.0000199738.37455.55.
OBJECTIVE/HYPOTHESIS: Nasal polyposis (NP) is a chronic inflammatory disease of the upper respiratory tract. The pathophysiology is unknown but has been shown to be multifactorial. Free radical-mediated damage has been implicated in the pathogenesis of NP. Superoxide dismutases (SODs) are the first and the most important line of antioxidant enzyme defense against reactive oxygen species. Moreover, isozymes of the SOD family are critical for modulating the activity of nitric oxide, a gaseous free radical that is believed to play roles in the physiology and pathology of respiratory tracts. However, the expression profile of SOD isoforms in NP remains unclear. We aimed to investigate the expression profile of the SOD isoforms in nasal polyps from nonallergic patients.
Prospective study.
Nasal polyp tissues were obtained from eight nonallergic patients who underwent elective polypectomy; mucosal specimens from the middle turbinates were acquired from eight subjects without NP as control tissues. The expression profile of SOD isoenzymes, SOD1, SOD2, and SOD3, in the nasal tissues was determined by reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blotting (WB).
NP in all eight of the NP patients manifested as severe or recurrent sinonasal polyposis clinically. The expression pattern of SOD isoenzymes evaluated by RT-PCR analysis indicated that the mean levels of SOD1 mRNA and, to a greater extent, SOD3 mRNA were higher in polyp tissues than in control tissues. There was no significant difference in the expression levels of SOD2 mRNA between the two groups. The data from ELISA and WB analysis showed that there were increased expressions of SOD1 and SOD3 protein in polyp tissues compared with the control tissues, but there was no difference in the expression of SOD2 protein between the two groups. The results from RT-PCR, ELISA, and WB were paralleled and revealed that the expressions of SOD1 and, to a greater extent, SOD3 were higher in polyp tissues than in the control group.
The expressions of SOD3 and SOD1 were higher in polyp tissues. These results are consistent with previously reported data and support the hypothesis that there is increased oxidative stress in NP. Our data also suggest that the SODs might be important in the pathogenesis of NP; however, the roles these SOD isoforms, especially SOD3, play in both normal nasal mucosa and NP require further clarification.
目的/假设:鼻息肉病(NP)是上呼吸道的一种慢性炎症性疾病。其病理生理学尚不清楚,但已表明是多因素的。自由基介导的损伤与NP的发病机制有关。超氧化物歧化酶(SODs)是对抗活性氧的第一道也是最重要的抗氧化酶防线。此外,SOD家族的同工酶对于调节一氧化氮的活性至关重要,一氧化氮是一种气态自由基,被认为在呼吸道的生理和病理过程中发挥作用。然而,NP中SOD同工型的表达谱仍不清楚。我们旨在研究非过敏性患者鼻息肉中SOD同工型的表达谱。
前瞻性研究。
从8例接受择期息肉切除术的非过敏性患者中获取鼻息肉组织;从8例无NP的受试者中获取中鼻甲黏膜标本作为对照组织。通过逆转录-聚合酶链反应(RT-PCR)、酶联免疫吸附测定(ELISA)和蛋白质印迹法(WB)测定鼻组织中SOD同工酶SOD1、SOD2和SOD3的表达谱。
所有8例NP患者的NP在临床上均表现为重度或复发性鼻-鼻窦炎息肉病。通过RT-PCR分析评估的SOD同工酶表达模式表明,息肉组织中SOD1 mRNA的平均水平,以及在更大程度上SOD3 mRNA的平均水平高于对照组织。两组之间SOD2 mRNA的表达水平无显著差异。ELISA和WB分析的数据显示,与对照组织相比,息肉组织中SOD1和SOD3蛋白的表达增加,但两组之间SOD2蛋白的表达无差异。RT-PCR、ELISA和WB的结果一致,表明息肉组织中SOD1的表达,以及在更大程度上SOD3的表达高于对照组。
息肉组织中SOD3和SOD1的表达较高。这些结果与先前报道的数据一致,并支持NP中氧化应激增加的假设。我们的数据还表明,SODs可能在NP的发病机制中起重要作用;然而,这些SOD同工型,尤其是SOD3,在正常鼻黏膜和NP中所起的作用需要进一步阐明。