Ultrastructural changes of penile tunica albuginea in diabetic rats

Aim: To clarify the ultrastructural changes of penile tunica albuginea (TA) in streptozotocin (STZ)-induced diabetic rats. Methods: Intraperitoneal injection of STZ was used to induce diabetes mellitus (DM) in 12 Sprague Dawley rats. Ten rats (age and weight-matched) were used as control. Blood samples from the tail snips of the rats were used for the determination of serum glucose levels with SureStep Plus Blood Meter. At week 4 and 10 after the injection, half of the rats in each group were sacrificed and penile samples were obtained from the middle third of the penile shaft for the examination of TA under scanning electron microscopy. Results: In the diabetic group, the serum glucose levels were higher (P＜0.01 at both time points) and the TA were thinner (P＜0.05) than those of the controls.In the control group, the fibers of TA were rich and arranged regularly and undulated, while in the diabetic group, the fibers were diminished, lost the undulations and were arranged irregularly. Conclusion: In rats, DM appeared to impair the penile TA ultrastructures and this impairment could contribute to diabetic erectile dysfunction in part by impairing the veno-occlusive function. (Asian J Andro12004 Dec;6:365-368)     

杜仲对糖尿病大鼠扑捉行为和阴茎组织神经传导通路的影响

目的:探讨杜仲改善勃起功能的药效和病理学机制。方法:雄性糖尿病(DM)大鼠30只随机分为3组:A组(10只,DM大鼠赋形剂灌胃组)、B组(10只,DM大鼠西地那非灌胃组)、C组(10只,DM大鼠杜仲灌胃组)及10只正常对照组大鼠(赋形剂灌胃,D组);灌胃4周后观察4组大鼠扑捉行为,透射电镜检查阴茎组织有髓神经纤维超微特征;用免疫组化二步法显示阴茎组织中神经元型一氧化氮合酶(nNOS)的表达。结果:与A组比较,C组大鼠扑捉次数显著增多(P<0.05),阴茎组织中nNOS表达显著增强(P<0.001)。透射电镜显示:A组大鼠阴茎组织有髓神经纤维排布失序,部分变性、板层分离形成透明空泡或网络状,C组大鼠有髓神经纤维排列规整,板层结构清晰。结论:杜仲可通过减轻有髓神经的损伤、增强阴茎组织中nNOS表达改善ED。     

糖尿病大鼠痛性周围神经病变时脊髓小胶质细胞的活化

目的 评价糖尿病大鼠痛性周围神经病变时脊髓小胶质细胞的活化.方法 SD大鼠25只,2月龄,雌雄不限,腹腔注射1%链脲佐菌素60 mg/kg以制备大鼠糖尿病痛性周围神经病变模型,取造模成功的10只SD大鼠作为糖尿病痛性周围神经病变组(DM组),另取10只同月龄SD大鼠作为对照组(NC组).分别于注射前(T1)、注射后2、7、14、21、28 d(T2～6)时称量体重,取尾静脉血0.1 ml测定血糖水平,于T1、T3～6时测定大鼠右后爪机械缩足反应阈值;注射28 d时麻醉大鼠,取L4.5脊髓制备切片,采用免疫组化法检测脊髓小胶质细胞补体受体3(CR3)的表达.结果 与NC组比较,DM组T2～6时血糖升高、体重下降,T4～6时机械缩足反应阈值降低,T6时小胶质细胞CR3表达上调(P<0.05或0.01);与T1时比较,DM组T2～6时血糖升高、体重下降,T6时机械缩足反应阈值降低(P<0.01).结论 脊髓小胶质细胞的活化与大鼠糖尿病痛性周围神经病变的发病有关.     

Antifibrogenic role of valproic acid in streptozotocin induced diabetic rat penis

We investigated the therapeutic effects of valproic acid (VPA) on erectile dysfunction and reducing penile fibrosis in streptozocin (STZ)‐induced diabetic rats. Eighteen male rats were divided into three experimental groups (Control, STZ‐DM, STZ‐DM plus VPA) and diabetes was induced by transperitoneal single dose STZ. Eight weeks after, VPA and placebo treatments were given according to groups for 15 days. All rats were anesthetised for the measurement of in vivo erectile response to cavernous nerve stimulation. Afterward penes were evaluated histologically in terms of immune labelling scores of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and transforming growth factor‐β1 (TGF‐β1). Slides were also evaluated in terms of collagen/smooth muscle ratio and penile apoptosis. After the treatment with VPA, erectile responses were found as improved when compared with STZ‐DM rats but not statistically meaningful. eNOS and VEGF immune expressions diminished in penile corpora of STZ‐DM rats and improved with VPA treatment. VPA led to decrease in TGF‐β1 expression and collagen content of diabetic rats’ penes. Penile apoptosis was not diminished with VPA. In conclusion, VPA treatment seems to be effective for reducing penile fibrosis in diabetic rats and more prolonged treatment period may enhance erectile functions.     

丙戊茶碱对糖尿病痛性周围神经病变大鼠脊髓星形胶质细胞活化的影响

目的 评价丙戊茶碱对糖尿病痛性周围神经病变大鼠脊髓星形胶质细胞活化的影响.方法 清洁级SD大鼠40只,月龄2月,雌雄不拘,体重180-200 g,腹腔注射1%链脲佐菌素60 mg/kg以制备大鼠糖尿病痛性周围神经病变模型.取模型制备成功的大鼠20只,随机分为糖尿病组(DM组)和丙戊茶碱组(PP组),每组10只;另取10只同月龄D大鼠作为对照组(NC组).PP组和DM组在注射链脲佐菌素后第28天开始,每天分别腹腔注射丙戊茶碱10 mg/kg和等容量生理盐水,注射1周.于注射链脲佐菌素前(TI)、注射链脲佐菌素后2、7、14、21、28、35 d(T2-7)时取尾静脉血样0.1 ml测定血糖水平;于T1、T3-7,时测定大鼠右后爪机械缩足反应阈值(PWT);T7时处死大鼠,取L4,s脊髓制备切片.采用免疫组化法检测神经胶质纤维酸性蛋白(GFAP)表达.结果 与TI时比较,DM组和PP组L2-7时血糖水平升高,T4-7时PWT降低(P<0.01);与NC组比较,DM组和PP组T2-7时血糖水平升高,T6,7时PWT降低,T7时GFAP表达上调(P<0.01);与DM组比较,T7时PWT升高,GFAP表达下调(P<0.05).结论 丙戊茶碱可能通过抑制脊髓星形胶质细胞活化减轻大鼠糖尿病神经病理性痛.     

Vascular endothelial growth factor restores erectile function through inhibition of apoptosis in diabetic rat penile crura

PURPOSE: Vascular endothelial growth factor (VEGF) is known as a multifunctional protein with roles in angiogenesis stimulation and apoptosis inhibition. We hypothesized that intracavernous administration of VEGF would recover erectile dysfunction due to diabetes by protection from apoptosis in the penile cavernosum. MATERIALS AND METHODS: A total of 30, 6-month-old male Sprague-Dawley rats were divided into 2 large groups, namely 20 with diabetes and 10 healthy controls. The diabetic group received intraperitoneal injection of streptozotocin (STZ) to induce diabetes. Intracavernous injection of VEGF was administered to randomly selected STZ diabetic rats 6 weeks after STZ injections. Erectile functional studies were performed in 10 STZ and 10 STZ plus VEGF rats at 12 weeks. After completion of the functional study the penile crura were collected for molecular and immunohistochemical studies. RESULTS: Mean intracavernous pressure in the diabetic group was significantly lower than in controls and low pressure was significantly recovered by VEGF treatment. Gene expression of pro-apoptotic and anti-apoptotic factors were present in the control, diabetic and VEGF treated groups. However, anti-apoptotic protein expression was lacking in the diabetic group and it was recovered by VEGF treatment. The apoptotic index in the diabetic group was significantly higher than in controls and this index was significantly decreased in the VEGF treated group. CONCLUSIONS: The decrease in and recovery of intracavernous pressure correlated significantly with a variation in anti-apoptotic protein expression in the diabetic and VEGF treated groups. To our knowledge this is the first study to show that intracavernous injection of VEGF restores erectile dysfunction through the inhibition of apoptosis in diabetic rats.     

2型糖尿病肾损害大鼠模型的建立

目的 在原有高糖高脂饮食+链脲佐菌素(STZ)造模方法的基础上进一步缩短造模时间,优化模型,使模型更加接近于人类2型糖尿病肾脏病,为探索其机制及治疗方法提供一个更好的动物模型.方法 将4周的雄性SD大鼠,随机分为正常饲料组(A组)和高糖高脂饲料+STZ组(B组).B组采用高糖高脂饲料+5%葡萄糖饮水喂养+STZ,诱发胰...     

Dietary resistant maltodextrin ameliorates testicular function and spermatogenesis in streptozotocin–nicotinamide‐induced diabetic rats

This study investigated the effect of resistant maltodextrin (RMD) on reproduction in streptozotocin (STZ)–nicotinamide‐induced type 2 diabetic male rats. Forty male rats were induced with diabetes by a single intraperitoneal injection of STZ (50 mg kg^?1) and nicotinamide (100 mg kg^?1). Five groups were analysed in total: normal, diabetic rats without RMD, diabetic rats with RMD 1.2 g per 100 g diet (1×), with RMD 2.4 g per 100 g (2×), and with RMD 6.0 g per 100 g (5×). The groups of diabetic rats with the RMD supplement, compared to those without supplement, showed improved plasma glucose control, attenuated insulin resistance and recovery of testosterone level and spermatogenesis stage. The STZ–nicotinamide‐induced diabetes mellitus (DM) caused a significant reduction in serum testosterone, testis androgen receptor (AR), steroidogenic acute regulatory protein (StAR) and 3β‐hydroxysteroid dehydrogenase (3β‐HSD) protein, but a statistical recovery in each of these was observed in the 5× group. TUNEL‐positive cells were observed in the diabetic without RMD group, and RMD treatment reduced apoptotic germ cells. The expression of Bax/Bcl2 was induced in the diabetic group and also significantly reduced in the 5× group. Dietary RMD may improve metabolic control in STZ–nicotinamide‐induced diabetic rats and attenuate hyperglycaemia‐related impaired male reproduction and testicular function.     

糖尿病大鼠甩尾潜伏期升高早期心脏感觉神经神经生长因子的表达变化

目的 观察糖尿病大鼠甩尾潜伏期(tail flick latency,TFL)升高早期上胸段背根神经节(dorsal root ganglion,DRG)、血清神经生长因子(nerve growth factor,NGF)含量变化. 方法 雄性SD大鼠18只,体重200～250 g,按随机数字表法分为对照组(C组,6只)和糖尿病组(DM组,12只).DM组大鼠经腹腔注射链脲佐菌素(streptozotocin,STZ)50 mg/kg.用疼痛甩尾仪每周测定大鼠TFL,监测躯体感觉神经病变的形成及变化.当DM组大鼠TFL显著升高时,取T1～T5节段DRG和血液样本,采用ELISA法测定标本中NGF水平. 结果 糖尿病造模5周末时,DM组大鼠TFL较C组显著升高.将TFL变化率＜100％的DM组大鼠设为DM1组(6只),TFL变化率≥100％的DM组大鼠设为DM2组(6只).NGF检测结果显示:与C组比较,DM1组DRG、血清中的NGF含量分别升高18％(P＜0.05)和16％(P＜0.05),DM2组DRG、血清中的NGF含量分别降低40％(P＜0.01)和14％(P＜0.05). 结论 糖尿病神经病变早期,随神经病变的加重,DRG、血清NGF含量表现为过表达和低表达,其机制和生物学意义值得进一步探讨.     

胰岛素对糖尿病大鼠阴茎内nNOS神经纤维的影响

目的探讨糖尿病性阴茎勃起功能障碍（ED）的发病机制及胰岛素的治疗作用。方法注射链脲佐菌素建立糖尿病（DM）大鼠模型，胰岛素治疗组于成模后注射胰岛素。7周和12周后注射阿扑吗啡（APO）进行大鼠阴茎勃起功能实验，取大鼠阴茎和血浆，用ABC免疫组织化学法观察nNOS神经纤维的变化。测定血浆NOS活性。结果（1）与对照组相比，DM组大鼠阴茎勃起次数明显减少;胰岛素治疗后症状缓解;（2）与对照组相比，DM组血浆NOS活性明显增高;DM组血浆NOS活性与病程延长呈负相关;与DM组比较，胰岛素治疗组血浆NOS活性明显降低;（3）与对照组相比，DM组阴茎内nNOS阳性神经纤维明显减少;与DM组比较，胰岛素治疗组nNOS阳性神经纤维表达增加。结论糖尿病性ED阴茎内nNOS阳性纤维的数量及光密度随DM病程的延长而下降;早期给予胰岛素治疗可预防糖尿病大鼠ED的出现及阴茎内nNOS含量的下降。     

Effects of diabetes on nitric oxide synthase and growth factor genes and protein expression in an animal model.

Erectile dysfunction occurs frequently in humans with diabetes mellitus; the molecular basis of this phenomenon is not known. We investigated the effects of diabetes on penile erection, nitric oxide synthase and growth factors expression in an animal model. Forty male rats were divided into two groups: the experimental group (n = 30) received intraperitoneal injection of Streptozotocin (STZ) dissolved in citrate buffer to induce diabetes; ten age-matched control rats received injection of citrate buffer vehicle only. Before euthanization at eight weeks, erectile function was assessed by electrostimulation of the cavernous nerves. NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. In the diabetic group, there was: (1) a significant decrease in NOS containing nerve fibers in the dorsal and intracavernosal nerves; (2) a significant lower maximal intracavernosal pressure. RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. These molecular changes may provide the basis for further studies to explore the association between diabetes and impotence.     

糖尿病肾脏病大鼠造模方法的改进及肾组织IL-10表达水平

目的对糖尿病肾脏病(diabetic kidney disease,DKD)大鼠造模方法进行改进并检测IL-10在肾组织的表达水平。方法48只雄性SD大鼠被随机分为正常对照组(NC组,n=24)、糖尿病(diabetes mellitus,DM)组(DM组,n=24),DM组以链脲佐菌素(streptozotocin,STZ)40 mg/kg一次性腹腔注射诱导DM模型。造模成功后分别于0周、4周、8周、12周检测血糖、尿糖、尿微量白蛋白、尿肌酐水平,观察大鼠肾脏病理在不同时间点的差别,应用免疫组化检测IL-10水平的表达。结果DM组大鼠造模成功率为75%,出现明显多饮、多食、多尿症状,至12周时,DM组大鼠平均体质量为(478.0±79.1)g,明显低于NC组(650.0±26.9)g;DM组大鼠血糖在造模成功后0周血糖(25.6±5.3)mmol/L显著高于NC组(5.2±0.2)mmol/L,直至实验结束发现血糖仍维持在(23.0±5.5)mmol/L;DM组大鼠尿微量白蛋白/尿肌酐比在8周、12周分别为(39.0±18.6)mg/g、(77.0±12.3)mg/g,均显著高于同期对照组(15.1±5.4)mg/g、(15.8±7.0)mg/g;光镜观察DM组大鼠0周即出现肾间质水肿、炎细胞浸润,第12周出现肾小球基底膜轻度增厚、肾小管上皮细胞空泡变性;免疫组化结果显示,NC组各期IL-10表达量均较DM组高。结论高糖高脂联合小剂量STZ建立DKD模型,在12周时肾脏才出现肾小球基底膜轻度增厚、肾小管上皮细胞空泡变性等病理改变,而不能单纯应用尾静脉血糖≥16.7 mmol/L判断DKD造模成功,肾组织IL-10表达降低进一步论证IL-10参与DKD发病并有可能作为DKD治疗的靶点。     

中电导型钙依赖钾通道在糖尿病大鼠阴茎海绵体中的表达及意义

目的 探讨糖尿病对大鼠阴茎海绵体中电导钙激活性钾通道蛋白(IKCa)表达的影响以及意义.方法 选用SD雄性大鼠35只,随机选择25只用于制作糖尿病动物模型,剩余10只用于空白对照.造模成功后饲养8周,注射阿朴吗啡(APO),观察大鼠阴茎勃起,同时采用逆转录-聚合酶链反应(RT-PCR)和Western blot技术检测IKCa mRNA和蛋白在大鼠海绵体的表达.结果 DM组大鼠阴茎勃起和IKCa mRNA及蛋白表达均显著低于STZ组和NDM组(P<0.05),STZ组和NDM组之间大鼠阴茎勃起情况和IKCa mRNA及蛋白表达无统计学意义(P>0.05).绪论糖尿病可降低大鼠阴茎勃起功能,IKCa在糖尿病大鼠海绵体表达明显降低.糖尿病对大鼠阴茎勃起功能的影响与阴茎海绵体IKCa表达减少密切相关.     

舒洛地特对糖尿病高血压大鼠足细胞podocalyxin表达的影响

目的 研究舒洛地特对糖尿病高血压大鼠的肾脏保护作用和足细胞podocalyxin（PCX）表达的影响。 方法 链脲佐菌素（STZ）注射后,醋酸脱氧皮质酮（DOCA）+盐建立糖尿病高血压大鼠模型。设对照组（CTL组）、模型组（STZ+DOCA组）、舒洛地特治疗组（GAG组）和舒洛地特+替米沙坦治疗组（GAG+ARB组）,每组各6只大鼠。于建模后0、2、4、6和8周测尾动脉压、尿白蛋白和8周末尿N-乙酰-β-葡萄糖苷酶（NAG）。8周末取血检测胰岛素、血肌酐（Scr）、胆固醇（TC）、三酰甘油 （TG）、Na+、K+。HE、PAS染色观察病理改变和肾小球正切面足细胞计数。免疫组织化学检测podocalyxin在肾小球表达和分布。RT-PCR和Western印迹法检测podocalyxin mRNA和蛋白表达。 结果 （1）GAG+ARB组4周末血压显著低于STZ+DOCA组和GAG组（P < 0.05）。GAG组和GAG+ARB组TG、TC和胰岛素与STZ+DOCA组差异无统计学意义。（2）6周末GAG+ARB组尿白蛋白量显著低于STZ+DOCA组 [（52.9±7.6） mg/24 h比（102.2±6.9） mg/24 h,P < 0.05];8周末GAG组和GAG+ARB组尿白蛋白量均显著低于STZ+DOCA组（P < 0.05）,而GAG+ARB组尿白蛋白量显著低于GAG组[（33.8±6.8） mg/24 h比(85.2±8.7) mg/24 h,P < 0.05]。GAG+ARB组和GAG组尿NAG均显著低于STZ+DOCA组（P < 0.05）。（3）GAG组和GAG+ARB组肾小球硬化指数（GSI）和间质纤维化指数（IF）均显著低于STZ+DOCA组（P < 0.05）,各组肾小球正切面足细胞数差异无统计学意义。（4）与STZ+DOCA组相比,GAG组PCX mRNA和蛋白表达显著增加,而GAG+ARB组PCX表达显著高于GAG组。 结论 舒洛地特可通过增加足细胞podocalyxin表达,减轻糖尿病高血压大鼠蛋白尿和病理损伤,与替米沙坦联用有叠加作用。     

GLP-1对2型糖尿病大鼠血清OPG、RANKL及骨密度的影响研究

目的探讨GLP-1类似物利拉鲁肽对糖尿病大鼠血清OPG、RANKL及骨密度的影响。方法健康雄性SD大鼠随机分为正常对照组(NC组)、糖尿病组(DM)、利拉鲁肽低剂量组(LR-L)、利拉鲁肽高剂量组(LR-H)。高脂高糖饮食联合小剂量链脲佐菌素(STZ)诱导建立2型糖尿病大鼠模型,低剂量组予利拉鲁肽400μg/(kg.d)皮下注射,高剂量组予利拉鲁肽800μg/(kg.d)皮下注射,给药4w后处死大鼠,测血糖、血钙、血磷、碱性磷酸酶、胆固醇、甘油三酯,ELISA法检测OPG、RANK,DXA法检测大鼠骨密度。结果与NC组比较,1 DM组、LR-L组、LR-H组体重均减轻,LR-L组、LR-H组较DM组更轻,但LR-L组与LR-H组间比较无差异;2DM组、LR-L组、LR-H组血糖均升高,LR-L组、LR-H组血糖较DM组低,但LR-L组与LR-H组间比较无差异;3DM、LR-H、LR-L组血清OPG、RANKL明显升高,差异具有统计学意义(P0.05),LR-L组OPG较DM组更高差异有统计学意义(P0.05),LR-H组OPG高于DM组但差异无统计学意义;LR-H与LR-L组RANKL明显低于DM组;4DM组血清OPG/RANKL比值低于NC组,LR-L、LR-H组血清OPG/RANKL较DM升高,差异具有统计学意义(P0.05);5DM组、LR-L、LR-H组大鼠全身及各部位骨密度均降低,差异具有统计学意义(P0.05),但DM组、LR-L组、LR-H组3组间差异无统计学意义。结论利拉鲁肽具有降低2型糖尿病大鼠体重、减低血清RANKL、升高血清OPG的作用,但利拉鲁肽治疗后未见骨密度的提高。     

神经生长因子在糖尿病神经病理性疼痛大鼠脊髓和背根神经节中的表达

目的 观察糖尿病早期大鼠脊髓背角及背根神经节神经生长因子(NGF)的表达及其与疼痛行为的相关性.方法 50只SD大鼠随机分为制模组(DM组,n=40)和止常对照组(C组,n=10).DM组又均分为制模1周组(DM1组)、制模2周组(DM2组)、制模4周组(DM4组)和制模8周组(DM8组)四个亚组.按55 mg/kg一次性腹腔注射链脲佐菌素(STZ)建立糖尿病大鼠模型.在制模前及制模后1、2、4、8周利用von Frey hairs测定大鼠机械痛阈,并通过蛋白质免疫印迹法测定每个时间点大鼠脊髓背角和背根神经节NGF的表达水平.结果 糖尿病大鼠机械痛阈在制模1周后即明显下降,并持续至8周;分别存制模2周和1周后脊髓背角和背根神经节内NGF表达水平出现显著下调,并分别持续至4周和8周.大鼠NGF表达水平与机械痛阈存在正相天性.结论 糖尿病早期大鼠外州及中枢神经系统NGF表达即出现下调,并与疼痛相关.     

Decreased fluidity of polymorphonuclear leukocyte membrane in streptozocin-induced diabetic rats

Using flow cytometry with the excimer-forming lipid technique with pyrenedecanoic acid, we measured membrane fluidity of polymorphonuclear leukocytes (PMNs) from 20 streptozocin (STZ)-induced diabetic rats. Diabetes mellitus was induced in male Sprague-Dawley rats (body wt 243 +/- 11 g) with an injection of 25 mg/kg i.v. STZ. Membrane fluidity of PMNs was significantly lower at 2 wk after the STZ injection when serum glucose reached the plateau (31.1 +/- 5.8 mM), and after 3 wk, membrane fluidity remained unchanged. In 7 STZ-resistant rats for which serum glucose was less than 10 mM at 2 wk after the STZ injection, gradual normalization in membrane fluidity was observed. PMN membrane fluidity at each week correlated inversely with respective serum glucose levels 1 wk previously (r = -0.76) but not with serum lipid levels. Cross-incubation studies ascribed this observation to factors in the diabetic rat serum. Glycosylated protein, which was separated from diabetic rat serum, decreased membrane fluidity of control rat PMNs. Human diabetic subjects have an increased risk for infection, which may be due partly to altered membrane fluidity of their PMNs.     

复方苍术汤对糖尿病大鼠肾脏非酶糖基化终末产物的影响

目的观察中药复方苍术汤对糖尿病大鼠肾脏非酶糖基化终末产物（AGEs）的影响。方法小剂量链脲佐菌素（STZ）注射加高糖高脂喂养建立糖尿病大鼠模型,给予复方苍术汤喂养8周,观察各组大鼠肾组织AGEs含量、肾重指数和空腹血糖的变化。结果复方苍术汤组大鼠的肾组织AGEs含量、肾重指数、血糖均较模型组降低（P〈0.01）。结论复方苍术汤降低糖尿病大鼠肾脏组织AGEs水平,其作用机制可能与降低血糖有关。     

舒洛地特对糖尿病大鼠肾脏病变的影响

目的:探讨2种剂量舒洛地特对糖尿病大鼠肾脏病变的影响。方法:采用STZ(链尿佐霉素,60mg/kg)腹腔注射法构建1型糖尿病大鼠模型,随机分为4组:糖尿病组(DM组)、舒洛地特10mg·kg-1·d-1组(S10组)、舒洛地特20mg·kg-1·d-1组(S20组)、氯沙坦30mg·kg-1·d-1组(L组),每组各10只。另取10只未造模大鼠作正常对照组(N组)。干预12周后测体重、24h尿白蛋白定量、血糖、血肌酐、尿素氮及肾重,光镜、电镜观察肾组织形态、结构的变化。结果:同N组相比,DM组大鼠24h尿白蛋白定量、血肌酐及尿素氮显著增加(P<0.01),病理改变较明显。同DM组相比,治疗组(S10、S20及L组)大鼠24h尿白蛋白定量减少(P<0.05或P<0.01),但血肌酐及尿素氮下降差异无统计学意义(P>0.05);同S10组相比,S20及L组大鼠24h尿白蛋白定量减少(P<0.05)。光镜及电镜显示治疗组较DM组病理变化减轻,尤以S20及L组病变减轻明显。结论:舒洛地特可对糖尿病大鼠有肾脏保护作用,而20mg·kg-1·d-1较10mg·kg-1·d-1的剂量效果更好。     

负压吸引对糖尿病性ED大鼠阴茎海绵体组织一氧化氮合酶表达的影响

目的研究负压吸引对糖尿病性勃起功能障碍（ED）大鼠阴茎组织一氧化氮合酶（NOS）表达水平的影响。方法25只实验鼠中随机选取5只为正常对照组（A组）,其余火鼠用链脲左菌素和阿朴吗啡诱导建立Ⅰ型糖尿病性ED大鼠模型。之后把造模成功的糖尿病性ED大鼠随机分成糖尿病ED吸引组（B组）和糖尿病ED非吸引组（C组）。在B组大鼠负压吸引治疗结束后将A、B、C3组大鼠处死并取阴茎组织进行石蜡包埋。采用免疫组织化学方法检测各组大鼠阴茎组织中三种一氧化氮合酶亚型（nNOS、eNOS、iNOS）的表达情况。结果A组大鼠阴茎组织中nNOS蛋白表达水平高于B组和C组（均P〈0.001）;A组和B组大鼠阴茎组织中eNOS蛋白表达水平高于C组（均P〈0.01）;A组iNOS蛋白表达水平低于B组和C组（P〈0.01,P〈0.001）,同时B组iNOS蛋白表达水平低于C组（P〈0.01）;剩余其他各组间的比较差异无统计学意义（P〉0.05）。结论负压吸引可以通过升高阴茎组织中的eNOS和降低iNOS的表达来改善勃起功能。