神经性勃起功能障碍大鼠阴茎海绵体内氧化应激状态研究

Oxidative stress status in corpus cavernosum tissue of neurogenic erectile dysfunction rats

目的：通过海绵体神经损伤建立神经性勃起功能障碍大鼠，研究其阴茎海绵体组织内氧化应激状态，及其对于大鼠阴茎勃起功能的影响。方法取成年雄性SD大鼠60只，随机分为3组：A组为假手术组（Sham组）， B组为单侧海绵体神经切断组，C组为双侧海绵体神经切断组。各组大鼠造模手术后8周，进行勃起功能试验后处死，取大鼠阴茎海绵体组织，测定大鼠阴茎海绵体组织中超氧化物歧化酶（SOD）水平、谷胱甘肽过氧化物酶（GSH-PX）及内皮型一氧化氮合酶（eNOS）活力，丙二醛（MDA）、一氧化氮（NO）含量，以及NADPH氧化酶gp91phox和p22phox亚基的mRNA表达情况。结果单侧海绵体神经损伤组和双侧海绵体神经损伤组的阴茎海绵体组织SOD水平、GSH-PX活性低于假手术组。单侧海绵体神经损伤组和双侧海绵体神经损伤组的阴茎海绵体组织MDA含量高于于假手术组。单侧海绵体神经损伤组和双侧海绵体神经损伤组的阴茎海绵体组织NO浓度和eNOS活力均低于假手术组。单侧海绵体神经损伤组和双侧海绵体神经损伤组的阴茎海绵体组织内NADPH氧化酶的gp91phox亚基和p22phox亚基mRNA的相对表达倍数均高于假手术组。结论通过对大鼠阴茎海绵体组织氧化应激相关指标（SOD、GSH-PX、MDA）、血管内皮功能相关指标（NO、eNOS）以及NADPH氧化酶功能亚基mRNA的相对表达倍数的测定，单侧海绵体神经损伤组和双侧海绵体神经损伤组的上述指标与假手术组之间均存在统计学差异，说明大鼠海绵体神经损伤致阴茎勃起功能障碍的过程中，除了本身神经损伤以外，阴茎海绵体组织的氧化应激以及NADPH氧化酶相关的阴茎海绵体血管内皮损伤也是大鼠神经性ED的发生、发展的重要机制之一。

Objective To investigate oxidative stress status in corpus cavernosum tissue of neurogenic erectile dysfunction rats. Methods Total of 60 male SD rats were divided them into three groupsincluding Group A （sham operated group）; Group B（ratswith one side of Cavernous nerve transection; Group C（ rats both sides of Cavernous nerve transection）. At the 8th weeks after surgery, rats received erectile function test and then were executed. Corpus cavernosum tissues of rats were collected. The levels of Superoxide Dismutase （SOD）, Malondialdehyde （MDA）, Nitric Oxide （NO）, vitality of Glutathione Peroxidase （GSH-PX） and Endothelial Nitric Oxide Synthase （eNOS）, and expression of NADPH oxidase subunits gp91phox and p22phox in corpus cavernosum tisues were measured. Results SOD level and vitality of GSH-PX in Group B and C were lower, than those in Group Awhereas level of MDA was higher. Also, the level of NO and vitality of eNOS in Group B and C were lower than those in Group A, but expressions of NADPH oxidase subunits gp91phox and p22phox were increased as compared with those of shamed operated group. Conclusion Theses results suggest that apart from nerve injury, oxidative stress of corpus cavernosum tissue and NADPH oxidase related Corpus cavernosum endothelial damage may also be major triggers for neurogenic erectile dysfunction of rats.