Daxx基因在小鼠睾丸精子发生过程中的表达特征

目的:研究死亡结构域相关蛋白(Daxx)基因在小鼠睾丸精子发生过程中的表达特征,初步探讨其在生精过程中的作用。方法:通过实时荧光定量PCR(q PCR)、Western印迹及免疫荧光等方法检测Daxx在不同周龄野生型小鼠睾丸组织以及成年睾丸支持细胞雄激素受体特异性敲除(SCARKO)和雄激素受体敲除(ARKO)小鼠睾丸中的表达特征。结果:q PCR、Western印迹和免疫荧光结果表明,Daxx基因在出生4周后小鼠睾丸中高表达,且主要定位于细胞核;与野生型小鼠相比,SCARKO小鼠睾丸中DAXX的表达差异不显著(0.853±0.058 vs1.000±0.015),但在生精细胞细胞核中呈极性分布;DAXX在ARKO小鼠睾丸表达显著降低(0.299±0.026 vs1.000±0.015,P0.01)。结论 :Daxx基因在小鼠睾丸发育中期时表达最高。ARKO小鼠中DAXX的表达与野生型相比显著降低,睾丸支持细胞中AR基因特异性敲除影响DAXX定位。DAXX可能参与调控小鼠的精子发生过程。     

过氧化物还原酶4在睾丸热应激时的保护作用

目的:以过氧化物还原酶4(PRDX4)基因全敲除(PRDX4~(-/y))小鼠为模型,研究PRDX4在睾丸热应激时的保护作用。方法:采用CRISPR/Cas 9技术对C57BL/6小鼠进行PRDX4基因全敲除,以野生型小鼠为对照,各24只。生长至性成熟(9周),PRDX4~(-/y)和野生型组各12只小鼠睾丸43℃水浴热应激15 min,1次/d,连续3 d;每组以25℃水浴作为热应激处理的对照。处理前、处理后1 d和处理恢复5周后,各组均分别处死4只小鼠,取双侧睾丸组织,采用HE染色观察组织学变化、TUNEL法检测细胞凋亡率、Western印迹检测PRDX4表达水平、免疫组化染色观察氧化应激因子(HNE和8-OHdG)表达水平。结果:与野生型小鼠比较,PRDX4基因全敲除小鼠的睾丸组织学、细胞凋亡和氧化应激因子表达差异不显著(P>0.05)。43℃水浴热应激处理后PRDX4~(-/y)小鼠[(38.65±2.57)%]和野生型小鼠[(13.21±1.434)%]生精细胞凋亡均显著升高(P<0.01),PRDX4~(-/y)小鼠生精细胞凋亡率增加2倍,5周后生精功能恢复较野生型差。热应激处理后,PRDX4~(-/y)小鼠睾丸8-OHdG(38.25±1.19)较野生型小鼠(24.30±1.65)表达水平显著增加(P<0.01),而两组HNE的表达水平无显著差异(P>0.05);恢复5周后,PRDX4~(-/y)小鼠生精细胞凋亡仍显著高于野生型小鼠[(3.09±0.16)%vs(1.45±0.11)%,P<0.01)],PRDX4~(-/y)小鼠睾丸生精细胞HNE的表达水平也高于对照组(28.57±0.56 vs 19±1.35,P<0.01),8-OHdG的表达水平也仍较对照组升高,但差异无显著性。结论:PRDX4在睾丸处于应激状态时具有重要的保护性作用,并促进睾丸生精功能恢复。     

去泛素化酶24基因在小鼠睾丸精子发生过程中的表达特征

目的:研究去泛素化酶24(USP24)基因在小鼠睾丸精子发生过程中的表达特征,初步探讨其在生精过程中的作用。方法:通过实时荧光定量PCR(qPCR)和免疫荧光等方法检测USP24在不同周龄野生型小鼠睾丸组织以及成年雄激素受体敲除(ARKO)小鼠睾丸中的表达特征;采用双荧光素酶报告基因实验检测USP24启动子转录活性。结果:qPCR和免疫荧光结果表明,USP24基因在出生1周时表达水平较低,3周时急剧升高,随后维持在相似水平至第8周;USP24主要定位于支持细胞和生精细胞的细胞质;与野生型相比,USP24在ARKO小鼠睾丸表达降低;性成熟小鼠睾丸中,USP24定位于成熟精子头部后端及中部。双荧光素酶报告基因实验结果显示,睾酮刺激后USP24启动子的转录活性升高。结论:USP24基因的表达水平的升高与小鼠的性发育相关,且其蛋白在小鼠成熟精子上表达。USP24是受雄激素受体(AR)调控的靶基因。USP24可能参与调控小鼠的精子发生过程。     

ACE2对5/6肾切除小鼠肾损伤的保护作用

目的:研究血管紧张素转换酶抑制剂(ACE2)在肾素血管紧张素系统(RAS)过度激活和进行性肾损害的作用并探讨其可能的作用机制。方法:选取雄性ACE2基因敲除(KO)小鼠及野生型(WT)小鼠,随机分成5/6肾脏切除模型组和假手术组,每2周测量血压,12周后检测肾脏损伤指标血肌酐,并对残余肾组织进行PAS染色观察病理变化;用RT-PCR检测肾组织纤维化指标α-SMA和炎症指标TNF-α的表达。结果:与野生型小鼠比较,ACE2基因敲除型小鼠出现血压明显升高,血肌酐增加。PAS染色分析结果提示ACE2基因敲除型小鼠较野生型出现更严重的系膜区增宽,系膜基质增生。用RT-PCR检测肾组织α-SMA和TNF-α的表达变化,提示ACE2基因敲除模型组小鼠肾脏纤维化和炎症因子的表达较野生型模型组小鼠显著增加。结论:ACE2基因敲除组小鼠较野生型小鼠在5/6肾脏切除术后出现更严重的肾脏损伤,血压增高,肾脏炎症和纤维化改变。     

TIPE2在小鼠脓毒症心肌损伤中的作用：与AKT/GSK-3β/β-catenin信号通路的关系

目的评价肿瘤坏死因子α诱导蛋白家族8样蛋白2(TIPE2)在小鼠脓毒症心肌损伤中的作用及其与丝氨酸苏氨酸蛋白激酶(AKT)/糖原合酶激酶3β(GSK-3β)/β-连环蛋白(β-catenin)信号通路的关系。方法选择16只雄性野生型C57BL/6N小鼠和16只雄性TIPE2基因敲除C57BL/6N小鼠, 6～8周龄, 体质量20～25 g, 按照随机数字表法分为野生型假手术组(WT-Sham组)、野生型CLP组(WT-CLP组)、TIPE2基因敲除型假手术组(WT-Sham组)和TIPE2基因敲除CLP组(KO-CLP组), 每组8只。采用盲肠结扎穿孔法制备脓毒症小鼠急性心肌损伤模型。术后24 h时采集下腔静脉血标本, 采用ELISA法检测血清心肌cTnI浓度, 然后处死小鼠, 取心肌组织, HE染色观察病理学结果, 采用q-PCR法检测TNF-α、IL-1β及IL-6的mRNA表达, Western blot法检测TIPE2、磷酸化AKT(p-AKT)、磷酸化(p-GSK-3β)及β-catenin表达。结果与相应Sham组比较, 相应CLP组血清cTnI浓度升高, 心肌组织TNF-...     

卵巢肿瘤结构域蛋白酶1在脓毒症小鼠急性肺损伤中的作用：与TAK1-MAPK信号通路的关系

目的评价卵巢肿瘤结构域蛋白酶1(OTUD1)在脓毒症小鼠急性肺损伤中的作用及其与转化生长因子β活化激酶1 (TAK1)-丝裂原活化蛋白激酶(MAPK)信号通路的关系。方法雄性野生型和OTUD1基因敲除的C57BL/6N小鼠各20只, 6～8周龄, 体质量20～25 g。采用随机数字表法分别分为野生型假手术组(WT-Sham组)、野生型脓毒症组(WT-SEP组)、OTUD1基因敲除型假手术组(KO-Sham组)和OTUD1基因敲除SEP组(KO-SEP组), 每组10只。采用盲肠结扎穿孔法制备脓毒症小鼠急性肺损伤模型。于术后24 h时处死小鼠, 采集腹主动脉血样, 取肺组织。采用血气分析仪行血气分析, 计算氧合指数(OI), 光镜下观察肺组织形态学并计算肺损伤评分, 确定肺组织湿重/干重(W/D)比值, 测定髓过氧化物酶(MPO)活性;采用ELISA法测定血浆TNF-α和IL-6浓度, Western blot法检测肺组织OTUD1、磷酸化(p-)TAK1、p38、c-Jun氨基末端激酶(JNK)和细胞外调节蛋白激酶(ERK)的表达。结果与WT-Sham组比较, WT-SEP组小鼠PaO...     

生精障碍BALB/c小鼠睾丸组织的体外培养研究

目的:探寻生精障碍小鼠睾丸组织生精能力的体外发育与成熟方法。方法:8周龄BALB/c雄性小鼠68只,随机分为4组,每组17只。对照组为正常同龄BALB/c雄性小鼠睾丸组织,实验组分别采用注射40 mg/kg白消安后第4周睾丸组织为SCOS组,第6周睾丸组织为重度H-S(H-S1)组,第8周睾丸组织为轻度H-S(H-S2)组。琼脂糖凝胶法体外培养3种生精障碍小鼠睾丸组织及对照组睾丸组织至第4周,通过免疫组化检测减数分裂过程中标记蛋白[减数分裂启动:维甲酸诱导蛋白8(STRA8);减数分裂中:联会复合蛋白3(SCP3);减数分裂后:转换蛋白1(TNP1)]的表达情况,判断体外培养过程中生殖细胞的发育与成熟能力; TUNEL法检测培养前后生殖细胞凋亡情况。结果:①培养前与对照组相比,睾丸组织损伤越严重其STRA8的表达越少(P0.05);随着培养时间的延长,在培养4周后3个实验组中STRA8的表达呈上升趋势(P0.05)。②培养前与对照组相比,SCOS组SCP3表达最少、H-S2表达最多(P0.05);培养4周后SCP3表达增加,但仍未达到对照组表达水平,且损伤越严重,表达越少;③培养4周后TNP1在对照组有阳性表达,H-S1、H-S2组可见个别阳性表达(P0.05),SCOS组无表达。④与培养前相比,培养4周后SCOS组凋亡增加,H-S组凋亡减少(P0.05)。结论:琼脂糖凝胶体外培养可以诱导生精障碍的BALB/c小鼠睾丸组织进行减数分裂,生精功能损伤较轻者的体外培养效果好。     

运动神经元生存蛋白基因敲除在顺铂致小鼠急性肾损伤中的作用

目的探讨运动神经元生存蛋白(survival motor neuron, SMN)基因敲除在顺铂诱导的急性肾损伤(acute kidney injury, AKI)小鼠中的作用。方法构建顺铂诱导的AKI小鼠(C57BL/6)模型, 将雄性8～10周龄体重22～24 gSMN+/+野生型小鼠及SMN基因敲除杂合子(SMN+/-)小鼠随机分为4组:SMN+/+生理盐水组(野生型空白对照组, n=5)、SMN+/-生理盐水组(SMN基因敲除杂合子空白对照组, n=5)、SMN+/+顺铂组(野生型顺铂组, n=5)和SMN+/-顺铂组(SMN基因敲除杂合子顺铂组, n=5)。腹腔注射20 mg/kg顺铂溶液或0.9%生理盐水, 72 h后处死小鼠, 收集血清及肾组织。采用实时荧光定量PCR和Western印迹法检测SMN mRNA和蛋白表达水平, 采用肌氨酸氧化酶法和脲酶法分别测定血清肌酐和尿素氮水平, PAS染色观察肾组织病理改变, TUNEL免疫荧光检测细胞凋亡水平, Western印迹和免疫组化法检测细胞凋亡标志蛋白多腺苷二磷酸核糖聚合酶(PARP)和内质网应激标志蛋白CHOP的表达。结...     

蛋白酶体REGγ对雄性小鼠生精功能的影响

目的研究蛋白酶体REGγ对雄性小鼠生精功能的影响。方法利用免疫蛋白印迹检测小鼠睾丸中REGγ的表达;通过组合酶消化法分离精原干细胞,流式细胞仪检测精原干细胞中c-kit及α6-integrin的表达;通过小鼠精子分析仪检测REGγ基因敲除雄鼠的精子浓度和精子活力;进行小鼠合笼实验检测正常雌鼠和REGγ基因敲除雄鼠合笼后的生育力。结果 REGγ在小鼠睾丸中高表达;应用组合酶消化法得到了纯度70%的精原干细胞;REGγ基因敲除雄鼠精原干细胞的c-kit及α6-integrin表达量均显著低于野生型组(P0.05);REGγ基因敲除型雄鼠的平均精子浓度(37.1×106/ml)和精子活力(54%)均显著低于野生型雄鼠(75.4×106/ml、74%)(P0.05);REGγ基因敲除型雄鼠与野生型雌鼠合笼后的产仔数均低于野生型雄鼠(P0.05)。结论蛋白酶体REGγ参与调节雄鼠的生精功能。     

睾丸移植物中支持细胞相关基因和蛋白表达的研究

目的 研究新生小鼠睾丸组织异体异位移植后,几种在睾丸支持细胞中起重要作用的基因和蛋白表达情况,为异体异位睾丸组织移植模型用于科研及临床的可行性提供进一步实验数据.方法 将162只1～2d昆明小鼠的睾丸移植到54只7～12周去势雄性免疫缺陷小鼠背部;在移植后9个时间段(3d和1～8周)取出移植物;选取4种在睾丸支持细胞中表达或高表达的基因abp、amh、vim和clu,采用聚合酶链反应,对发育不同阶段移植物中4种基因的表达情况进行分析,并与正常小鼠相应各年龄段睾丸中的基因表达相比较;同时采用免疫组织化学方法对支持细胞的GATA-4蛋白在移植物组织中的表达量及分布情况进行分析.结果 在9个时间段取出的移植物中,所测定4种基因的表达趋势与在正常小鼠睾丸中所见基本相同;免疫组化结果显示,4周和8周移植物支持细胞中GATA-4蛋白呈高表达,与在正常小鼠睾丸组织支持细胞中的表达基本一致.结论 新生小鼠睾丸组织异体异位移植到免疫缺陷小鼠体内后,支持细胞的发育在组织形态学以及几种受试基因的表达趋势和蛋白的表达情况与在正常小鼠中的表现基本相同.     

Limbic epileptogenesis in a mouse model of fragile X syndrome

Fragile X syndrome (FXS), caused by silencing of the Fmr1 gene, is the most common form of inherited mental retardation. Epilepsy is reported to occur in 20-25% of individuals with FXS. However, no overall increased excitability has been reported in Fmr1 knockout (KO) mice, except for increased sensitivity to auditory stimulation. Here, we report that kindling increased the expressions of Fmr1 mRNA and protein in the forebrain of wild-type (WT) mice. Kindling development was dramatically accelerated in Fmr1 KO mice, and Fmr1 KO mice also displayed prolonged electrographic seizures during kindling and more severe mossy fiber sprouting after kindling. The accelerated rate of kindling was partially repressed by inhibiting N-methyl-D-aspartic acid receptor (NMDAR) with MK-801 or mGluR5 receptor with 2-methyl-6-(phenylethynyl)-pyridine (MPEP). The rate of kindling development in WT was not effected by MPEP, however, suggesting that FMRP normally suppresses epileptogenic signaling downstream of metabolic glutamate receptors. Our findings reveal that FMRP plays a critical role in suppressing limbic epileptogenesis and predict that the enhanced susceptibility of patients with FXS to epilepsy is a direct consequence of the loss of an important homeostatic factor that mitigates vulnerability to excessive neuronal excitation.     

Ketamine/xylazine attenuates LPS-induced iNOS expression in various rat tissues

Ketamine and xylazine (K/X) are commonly used in combination as an anesthetic agent in experimental animal models. We previously noted that K/X attenuated lipopolysaccharide (LPS)-induced liver injury, gastric stasis, and reduced symptoms of endotoxemia. Because ketamine attenuates expression of several proinflammatory genes, we examined the effects of K/X on inducible nitric oxide synthase (iNOS), which has been implicated in endotoxin-induced tissue injury. We hypothesized that K/X would attenuate LPS-induced expression of iNOS in various organs in the rat. Rats were given either intraperitoneal saline or ketamine (70 mg/kg) and xylazine (6 mg/kg) 1 h before saline or LPS (20 mg/kg). Rats were sacrificed 5 h later and stomach, duodenum, jejunum, ileum, colon, liver, lung, kidney, and spleen were collected for determination of iNOS protein immunoreactivity by Western immunoblot. Data reported in densitometric units (DU) as mean +/- SEM (n >/= 5; ANOVA). LPS significantly increased iNOS protein immunoreactivity in all tissues examined versus saline controls (P 相似文献   

GATA-4在小鼠睾丸中的表达定位研究

目的:观察小鼠睾丸内GATA-4免疫反应产物的特征与分布。方法:选取刚出生、2、4、6周雄性B6SJLF1/J小鼠各6只,取睾丸进行石蜡切片,应用免疫组化ABC法,DAB显色,观察GATA-4在不同时期睾丸中的表达情况。结果:GATA-4免疫反应产物在以上4个阶段小鼠睾丸Sertoli细胞、Leydig细胞均有分布,且4、6周组小鼠睾丸Leydig细胞阳性率比刚出生和2周组小鼠更高(P<0.01);但4、6周组小鼠,除以上两种细胞外,生精细胞中也有分布,6周组小鼠比4周组小鼠阳性细胞率高(P<0.01)。结论:小鼠睾丸内存在GATA-4,为研究GATA-4在睾丸性别决定和分化以及激素调控方面提供了形态学依据。     

饮酒对大鼠生精细胞iNOS,Bcl-2基因表达的影响

目的 探讨酒精对大鼠睾丸诱导型一氧化氮合酶（iNOS）、Bcl-2基因表达和生精细胞凋亡的影响。方法30只成年健康SD雄性大鼠随机均分为对照组、低剂量组和高剂量组，用不同剂量的酒精灌胃成年大鼠26d（两个生精周期）后，免疫组织化学法（SP法）检测睾丸iNOS、BCl-2基因表达的变化；原位缺口末端标记法（TUNEL法）检测细胞凋亡指数（A1）的变化。结果 与对照组相比，低剂量组大鼠睾丸iNOS、Bcl-2基闪表达强度和细胞凋亡指数（A1）无明显变化（P〉0．05）：而高剂量组与对照组和低剂量组相比，iNOS表达显著增强（P〈0．01），Bcl-2基因表达明显减弱（P〈0．01，P〈0．05），细胞凋亡指数则增加（P〈0.01）。结论 长期大量饮酒可以诱导睾丸生精细胞凋亡增加，iNOS与Bcl-2基因表达的改变是重要原因之一。     

贫铀对大鼠睾丸诱导型一氧化氮合酶基因表达的影响

目的:通过研究贫铀(DU)颗粒气管灌注后大鼠睾丸诱导型一氧化氮合酶(iNOS)基因表达的变化,揭示DU对生殖系统的毒性作用机制。方法:W istar大鼠随机分为气管灌注生理盐水对照组和DU 1、3、5 mg组,每组5只。3个月后提取大鼠睾丸总RNA进行逆转录聚合酶链反应(RT-PCR)。凝胶成像分析系统扫描RT-PCR产物,用内参半定量法分析iNOSmRNA的变化。结果:对照组无iNOSmRNA表达,各染铀组扩增产物电泳条带吸光度A值明显高于对照组(P<0.05),其中3 mg组产物电泳条带A值最高,5 mg组A值明显低于1 mg组和3 mg组(P<0.05)。结论:DU颗粒气管灌注能使大鼠睾丸iNOSmRNA表达水平升高,DU剂量增高到一定程度则使iNOSmRNA表达水平降低,这种变化可能与DU化学毒性和辐射损伤的复合作用有关。     

Inducible nitric oxide synthetase is expressed in adult but not fetal pig pancreatic islets

Abstract: Cytokine-induced expression of inducible nitric oxide synthetase (iNOS) and production of nitric oxide (NO) by pancreatic islet cells has been suggested as one potential mechanism for beta cell destruction. In this study, we investigated the role of iNOS and NO in islet primary non-function. Islets were assessed for their function, viability and expression of iNOS. Adult rat and pig islets isolated by collagenase digestion and fetal pig pancreas (FPP) grafts isolated by collagenase digestion or high oxygen culture were transplanted into C57BL6 mice and nude mice. iNOS protein was detected by immunohistochemistry. iNOS protein was found in normal rat and pig pancreas and adult rat and pig islets that were isolated by collagenase digestion and transplanted into either C57BL6 mice or nude mice. iNOS was not detected in fetal pig islet grafts, regardless of whether collagenase was used in the isolation process. In adult pig islet grafts, the presence of iNOS protein correlated with high levels of islet cell apoptosis and primary non-function. Despite the persistent presence of iNOS in rat islets, there was no evidence that it had a deleterious effect on rat islet viability, or function. Therefore, in isolated adult pig islets, there was a correlation between iNOS expression and apoptosis, suggesting that iNOS activation may be deleterious to the adult pig islets. However, other factors such as the fragility of the islet capsule may be equally important. By contrast, fetal pig islets did not express iNOS and this may be an important reason for their enhanced viability when compared with adult islet tissue.     

Downregulation of tonic GABAergic inhibition in a mouse model of fragile X syndrome

The absence of fragile X mental retardation protein results in the fragile X syndrome (FXS), a common form of mental retardation associated with attention deficit, autistic behavior, and epileptic seizures. The phenotype of FXS is reproduced in fragile X mental retardation 1 (fmr1) knockout (KO) mice that have region-specific altered expression of some gamma-aminobutyric acid (GABA(A)) receptor subunits. However, little is known about the characteristics of GABAergic inhibition in the subiculum of these animals. We employed patch-clamp recordings from subicular pyramidal cells in an in vitro slice preparation. In addition, semiquantitative polymerase chain reaction and western blot experiments were performed on subiculum obtained from wild-type (WT) and KO mice. We found that tonic GABA(A) currents were downregulated in fmr1 KO compared with WT neurons, whereas no significant differences were observed in phasic GABA(A) currents. Molecular biology analysis revealed that the tonic GABA(A) receptor subunits alpha5 and delta were underexpressed in the fmr1 KO mouse subiculum compared with WT. Because the subiculum plays a role in both cognitive functions and epileptic disorders, we propose that altered tonic inhibition in this structure contributes to the behavioral deficits and epileptic activity seen in FXS patients. This conclusion is in line with evidence implicating tonic GABA(A) inhibition in learning and memory.     

Low androgen status inhibits erectile function by up-regulating the expression of P2X receptors in rat corpus cavernosum

The aim of our study was to investigate whether low androgen level inhibits the erectile function of rats by regulating the expression of P2X receptors. Thirty-six 8-week-old male SD rats were randomly divided into six groups: sham-operated groups (4w-sham, 8w-sham), castration groups (4w-cast, 8w-cast) and androgen replacement after castration groups (4w-cast + T, 8w-cast + T). The maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP), the levels of serum testosterone (T) and nitric oxide (NO), and the expression of P2X1, P2X2, P2X3, eNOS, p-eNOS, ROCK1 and ROCK2 in the cavernous tissue of rats were determined. The serum T, ICPmax/MAP and NO levels in penile corpus cavernosum in the castration groups were significantly lower than those in other groups (p < .01). The protein expression of P2X1, P2X2, P2X3, ROCK1 and ROCK2 in the castration groups was significantly higher than those in other groups (p < .01). P-eNOS/eNOS of the castration groups were significantly lower than those of other groups (p < .01). The serum T level was negatively correlated with the expression of P2X1, P2X2 and P2X3 in the corpus cavernosum. Low androgen level inhibits erectile function by up-regulating the expression of P2X1, P2X2, P2X3 and RhoA/Rho-kinase resulting in reducing the ratio of p-eNOS/eNOS and the level of NO in corpus cavernosum of rats.     

Propofol reduces nitric oxide-induced apoptosis in testicular ischemia-reperfusion injury by downregulating the expression of inducible nitric oxide synthase

Background: The aim of the present study was to investigate the underlying mechanisms in the preventive effects of intravenous anesthetics on testicular ischemia–reperfusion injury.
Methods: Forty male Wistar Albino rats were randomly assigned to four groups of 10 rats each. Anesthesia was induced and maintained with thiopental in groups 1 and 2 and with propofol in groups 3 and 4. Groups 2 and 4 received left testicular ischemia (torsion) for 1 h and reperfusion (detorsion) for 24 h. Groups 1 and 3 (control groups) had no testicular torsion and detorsion. At 24 h of reperfusion, animals were killed and ipsilateral testes were removed for determination of tissue nitric oxide (NO) levels and immunohistochemical evaluation of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and apoptosis protease-activating factor 1 (APAF-1).
Results: Between groups 1 and 3, there were no differences in tissue NO levels and eNOS, iNOS, and APAF-1 expressions. iNOS and APAF-1 expressions were markedly increased in group 2, but these parameters were at the mild to moderate level in group 4 at 24 h of reperfusion. Also, elevated expression of iNOS was accompanied by a high NO production in group 2 compared with group 4. Although eNOS expressions were increased in both the groups (groups 2 and 4), there were no significant differences between these groups.
Conclusions: Propofol as an anesthetic agent may attenuate germ cell-specific apoptosis and decrease NO biosynthases through downregulation of iNOS expression in an animal model of testicular torsion and detorsion.