This study compared tankyrase 1 expression and autophagy quantity between erectile dysfunction （ED） and non-ED rats＇ corpus cavernosum smooth muscle cells （CSMCs）. This study aslo explored the effect and possible mechanism of tankyrase 1 on autophagy and cell proliferation in ageing ED rats＇ CSMCs. The intracavernous pres- sure and mean systemic arterial pressure were measured to investigate erectile function so that eight 24-month-old ED and eight 8-month-old male Wistar rats were choosed respectively. The rat CSMCs were isolated and cultured by enzyme digestion, in which tankyrase 1 expression and autophagy quantity were compared. Tankyrase 1 over-expression was induced with plasmid transfection by Lipofectamine^TM. The effect of tankyrase 1 overexpression on proliferation, autophagy and mTOR pathway in 24-month-old ED rats＇ CSMCs was measured by the cell growth curve in MTT assay, cell cycle analysis in flow cytometry （FCM）, key protein expression in Western blot, autophagy quantity in transmission electron microscopy, monodansylcadaverine staining and GFP-LC3 fluorescence. The primary CSMCs were confirmed by immunofluorescence, and the purity was 99.1% in FCM. Compared with that of 8-month-old rats, tankyrase 1 expression and autophagy quantity significantly decreased in 24-month-old ED rats＇ primary CSMCs （P 〈 0.01）. Tankyrase 1 overexpression significantly increased the growth rate （P 〈 0.05） and increased the S phase of cell cycle （P 〈 0.01）. The autophagosome quantity was remarkably increased （P 〈 0.01）, LC3-Ⅰ/Ⅱ and Beclin 1 were upregulated （P 〈 0.01 and P 〈 0.05）, and p-p70S6K （Thr389） was downregulated in 24-month-old ED rat CSMCs （P 〈 0.05）. In conclusion, Tankyrase 1 and autophagy decrease in the CSMCs from aging rats with ED, and tankyrase 1 may have a positive effect on proliferation by enhancing autophagy and regulating the mTOR signalling pathway.
目的:观察阴茎起勃器植入术(penile prosthesis implantation,PPI)治疗中国重度勃起功能障碍(severeerectile dysfunction,SED)患者的远期效果及患者和其配偶满意度。方法:自2000年7月至2010年6月,168例SED患者按照手术规范实施PPI治疗,术后随访6个月及6个月以上的患者146名(86.9%),其中植入三件套可膨胀性阴茎起勃器(AMS700CXM)110例(75.3%),植入单件套可屈性阴茎起勃器(AMS650)36例(24.7%)。随访时间6～119个月(平均82.1个月)。利用国际勃起功能评分表(international index of erectile function5,IIEF5)及生活质量评分表(quality of life,QOL)评估PPI术后效果,利用视觉模拟量表(visual analogue scale,VAS)评估患者和配偶满意度,并进行统计学分析。结果:SED患者146例,平均年龄(35.9±12.1)岁(20～75岁);PPI术后4～6周开始性生活,未见发生感染和糜烂等严重并发症。IIEF5和QOL评分分别为21.3±1.6和1.5±0.5,比较术前(6.3±1.7和5.1±0.9)两者均得到改善(P<0.01),植入AMS650和AMS700CXM两组之间差异无统计学意义(P>0.05)。PPI术后阴茎起勃器无故障者和每月两次以上性生活者分别为98.6%和87.9%。患者及其配偶对PPI的总体满意度分别达92.5%和90.4%,其中植入AMS700CXM患者满意度优于植入AMS650患者满意度(P<0.05)。结论:PPI治疗中国SED患者可显著改善其勃起功能和生活质量,其并发症发生率也较低,植入AMS700CXM患者满意度优于植入AMS650患者。
目的研究非梗阻性无精症(NOA)睾丸基因表达谱变化,为研究其发病机制奠定基础。方法知情同意下获取正常青年人和NOA患者的睾丸活检标本各3例,采用Q IA GEN RNA提取试剂盒提取总RNA,分别等量混合后制备探针。利用ClonTech公司生产的包含8000个已知基因的人类cDNA基因芯片[Atlas Plastic Human 8K Mi2croarray(Cat.#790521)]筛选差异表达基因。按基因功能分类方法对睾丸组织中差异表达的基因进行归类分析。从基因芯片结果中选择我们感兴趣的基因用RT-PCR、T-A克隆测序方法验证。结果筛选到显著差异表达基因4117个(上调基因1564个,下调基因2553个)。在表达上调的基因中代谢相关基因(11.4%),与基因和蛋白表达相关的基因(34.8%),信号通路相关基因(28.3%),细胞分化相关基因(16.5%),细胞结构和运动相关基因(4.2%),细胞或内环境稳态相关基因(24.9%)。在表达下调的基因中代谢相关基因(13.6%),与基因和蛋白表达相关的基因(31.5%),信号通路相关基因(36.7%),细胞分化相关基因(13.5%),细胞结构和运动相关基因(3.6%),细胞或内环境稳态相关基因(20.1%)。RT-PCR及T-A克隆测序进一步证实TGF-β信号通路中TGFβRⅡ和Smad2基因在NOA患者睾丸组织显著上调。结论NOA患者睾丸组织中基因表达谱发生了明显变化,NOA与多种基因表达变化有关,其中TGF-β信号通路显著上调可能对进一步研究NOA的机制具有重要意义。
Premature ejaculation （PE） is a common sexual disorder in men that is mediated by disturbances in the peripheral and central nervous systems. Although all pharmaceutical treatments for PE are currently used ＇off-label＇, some novel oral agents and some newer methods of drug administration now provide important relief to PE patients. However, the aetiology of this condition has still not been unified, primarily because of the lack of a standard animal model for basic research and the absence of a widely accepted definition and assessment tool for evidence-based clinical studies in patients with PE. In this review, we focus on the current therapeutic strategies and future treatment perspectives for PE.
Zhong-Cheng XinYi-Chen ZhuYi-Ming YuanWan-Shou CuiZhe JinWei-Ren LiTao Liu
