P47phox调控氧化应激干预代谢综合征大鼠勃起功能的实验研究

代谢综合征（MetS）是勃起功能障碍（ED）的重要危险因素之一，但是目前对MetS导致ED的机制尚不明确，尚无特异性针对MetS诱导ED的治疗方法。阴茎局部的氧化应激是MetS诱导ED的一个重要机制，而NADPH氧化酶能催化阴茎局部产生大量活性氧，使阴茎局部发生氧化应激。NADPH氧化酶亚基P47phox在上调NADPH氧化酶活性上发挥重要作用。本项目首次以阴茎组织中NADPH氧化酶亚基P47phox作为研究对象，在整体、离体、分子水平，探索阴茎组织中P47phox在MetS诱导ED中的作用机制，并针对该亚基应用RNA干扰技术下调其在阴茎中的表达，在整体、离体、细胞水平观察其治疗MetS诱导ED的效果。本项目有望阐明阴茎组织中P47phox通过上调NADPH氧化酶活性在MetS诱导ED发生中发挥重要作用，为临床治疗MetS诱导的ED 提供新的策略。

Metabolic syndrome is one of important risk factors of erectile dysfunction. The underlying mechanisms by which metabolic syndrome causes erectile dysfunction are remain unclear. At present,there is no specific therapy for erectile dysfunction induced by metabolic syndrome.Excessive reactive oxygen species in penis causes oxidative stress, which plays an important role in the pathogenesis of erectile dysfunction induced by metabolic syndrome. It has been well established that enhanced NADPH oxidase activity contributes to the development of oxidative stress in penis. P47phox,which is one of subunits NADPH oxidase, is crucial for NADPH oxidase activity. The purpose of our study is to explore the role of P47phox in penis in metabolic syndrome-induced erectile dysfunction. Furthermore,the penis tissue with knockdown P47phox expression by RNA interference was used to treat metabolic syndrome-induced erectile dysfunction in vivo and in vitro. Our study may demonstrate enhanced NADPH oxidase activity by P47phox in penile tissue is an important mechanism in the pathogenesis of erectile dysfunction induced by metabolic syndrome,by which would develop a new therapy to treat metabolic syndrome-induced erectile dysfunction.