目的：运用Meta分析研究GNB3基因C825T位点多态性与勃起功能障碍的相关性。方法检索Pubmed、Medline、中国期刊网全文数据库（CNKI）、万方数据库和维普中文科技期刊库，按照纳入标准纳入文献，对文献进行资料提取后，运用STATA 12.0软件进行Meta分析。结果共纳入4篇研究，包括969例ED患者和795例对照。采用共显性模型进行Meta分析，结果显示CC基因型较TT基因型与勃起功能障碍发病无显著关联（OR=0.639，95%CI：0.386-1.059，P =0.083）；对不同人群进行亚组分析提示亚组人群CC基因型较TT基因型勃起功能障碍患病风险增加；欧洲人群GNB3基因C825T位点基因多态性与勃起功能障碍无明显关联（CC vs TT， OR=1.043，95%CI：0.602-1.810，P=0.88； CT vs TT，OR=0.989，95%CI：0.568-1.723，P=0.97）。结论亚洲人群GNB3基因CC基因型为勃起功能障碍的危险因素，而在欧洲人群中关联尚不明确。
Silent information regulator 2-related enzyme 1(SIRT1)is an aging-related protein activated with aging.Herein,we evaluated the role of SIRT1 in aging-related erectile dysfunction.The expression of SIRT1 was modulated in aged Sprague-Dawley rats following intragastric administration of resveratrol(Res;5 mg kg^(-1)),niacinamide(NAM;500 mg kg^(-1))or Res(5 mg kg^(-1))+tadalafil(Tad;phosphodiesterase-5[PDE5]inhibitor;5 mg kg^(-1))for 8 weeks.Then,we determined erectile function by the ratio of intracavernosal pressure(IcP)/mean systemic arterial pressure(MAP).Cavernosal tissues were extracted to evaluate histological changes,cell apoptosis,nitric oxide(NO)/cyclic guanosine monophosphate(cGMP),the superoxide dismutase(SOD)/3,4-methylenedioxyamphetamine(MDA)level,and the expression of SIRT1,p53,and forkhead box O3(FOX03a)using immunohistochemistry,terminal deoxynucleotidyl transferase(TdT)-mediated 2'-deoxyuridine 5'-triphosphate(dUTP)nick-end labeling(TUNEL),enzyme-linked immunosorbent assays,and western blot analysis.Compared with the control,Res treatment significantly improved erectile function,reflected by an increased content of smooth muscle and endothelium,NO/cGMP and SOD activity,and reduced cell apoptosis and MDA levels.The effect of Res was improved by adding Tad.In addition,the protein expression of SIRT1 was increased in the Res group,accompanied by decreased p53 and FOxO3a levels.In addition,inhibition of SIRT1 by NAM treatment resulted in adverse results compared with Res treatment.SIRT1 activation ameliorated aging-related erectile dysfunction,supporting the potential of SIRT1 as a target for erectile dysfunction treatment.
