雄性大鼠

摘要： 目的 研究生命早期应激对青春期雄性大鼠下丘脑-垂体-性腺轴的影响.方法 将SD孕鼠随机分为对照组和模型组,每组4只.对照组孕鼠所产雄性仔鼠(n=28)和模型组孕鼠所产雄性仔鼠(n=26)用于实验.模型组孕鼠产雄性仔鼠出生后第2至9天(PND2～9)给予限制筑窝材料和垫料的应激,对照组孕鼠所产雄性仔鼠正常饲养.PND2至PND21检测两组仔鼠体重和尾长变化.PND21行旷场试验,PND22时部分大鼠腹腔注射水合氯醛麻醉,腹主动脉取血,放射免疫法检测血清皮质酮水平.PND42称量剩余大鼠体重,麻醉取血,解剖并收集大鼠睾丸,称量睾丸湿重并计算睾丸指数,HE染色法观察大鼠睾丸组织结构,放射免疫法检测大鼠血清性激素水平.结果 与对照组相比,模型组仔鼠PND2至PND21体重增加和尾长增长均显著减慢(P＜0.05);PND21自主活动显著减少[水平运动得分(11.7±7.1)vs.(48.7±11.2),垂直运动得分(0.8±0.5)vs.(5.9+1.7)](P＜0.05),修饰持续时间[(19.42+3.47)s vs.(6.79±2.00)s]显著增加(P＜0.01),表现出抑郁焦虑状态;PND22的血清皮质酮水平显著下降[(20.00±1.14)ng/ml vs.(23.14+2.46)ng/ml](P＜0.001).PND42模型组大鼠体重、睾丸湿重及睾丸指数均显著低于对照组(P＜0.05),显微镜下睾丸组织形态结构发生明显变化,生精小管间连接疏松,间质细胞数量减少;模型组大鼠的血清促性腺激素释放素(GnRH)[(60.99±4.27)vs.(56.40±4.81)pg/ml]和黄体生成素(LH)水平[(6.16±1.71)vs.(4.02±1.90)U/L]显著上升,而雌二醇(E2)[(29.83±2.78)vs.(39.02±10.60)pmol/L]和睾酮(T)水平[(0.72±0.45)vs.(1.50±0.84)nmol/L]显著下降(P均＜0.05).结论 生命早期应激可造成青春期雄性大鼠的生殖系统损伤,并导致下丘脑-垂体-性腺轴的功能失调.

摘要： 目的 研究黄芪总皂苷对运动性疲劳雄性大鼠生殖激素的调控作用和可能机制.方法 36只雄性SD大鼠随机分为正常组、模型组和给药组(黄芪总皂苷)三组.给药组以50 mg/kg黄芪总皂苷灌胃,正常组和模型组以等量生理盐水灌胃,每天1次.模型组和给药组大鼠在灌胃1h后进行中等强度的水平跑台运动,每天1次,连续14天,正常组常规饲养.在实验最后一天断头取血,检测血清睾酮(T)、卵泡刺激素(FSH)和黄体生成素(LH)含量,血清和下丘脑促性腺激素释放激素(GnRH)含量,下丘脑谷氨酸(Glu)和 γ-氨基丁酸(GABA)含量的变化.结果 和正常组比较,模型组大鼠血清T含量、下丘脑GnRH和Glu含量显著降低,血清FSH、GnRH和下丘脑GABA含量显著升高;和模型组比较,给药组大鼠血清T和LH含量、下丘脑GnRH和Glu含量显著升高,血清FSH、GnRH和下丘脑GABA含量显著降低.结论 黄芪总皂苷通过纠正中枢Glu和GABA代谢失衡的情况,改善HPG轴抑制状态,从而调节运动性疲劳状态下外周生殖激素水平紊乱的情况,对机体生殖系统起到保护作用.

摘要： 目的:探讨不同剂量的牡蛎低聚肽(OOP)对男性雄激素部分缺乏综合征(PADAM)大鼠性功能和生殖功能的干预作用.方法:将雄性SD大鼠随机分为正常对照组(NC组)、PADAM组(PC)、PADAM+低、中和高剂量OOP组(PLO、PMO、PHO)5组.除NC组外,其余大鼠在利用环磷酰胺诱导PADAM形成的同时补充不同剂量的OOP,6周后测定血清睾酮(TT)、游离睾酮(FT)、黄体生成素(LH)、卵泡刺激素(FSH)和睾丸雄激素受体(AR)含量、捕捉潜伏期、交配潜伏期、捕捉次数、交配次数以及附睾中的精子数量、活率和活力.结果:与NC组相比,PC组血清TT、FT、LH含量、交配次数以及精子数量、活率和活力均显著降低(P＜0.05),捕捉潜伏期和交配潜伏期显著延长(P＜ 0.05).与PC组相比,PLO组捕捉潜伏期显著缩短(P＜0.01)、捕捉和交配次数显著增多(P＜0.01);除PMO组精子数量无显著性增加外(P＞0.05),PMO和PHO组血清TT、FT、FSH、LH和睾丸AR含量以及捕捉和交配次数、精子数量、活率和活力显著增加(P＜0.05),捕捉和交配潜伏期显著缩短(P＜0.05),且PMO和PHO组血清TT、FSH含量和交配次数以及PHO组血清LH和睾丸AR含量显著高于PLO组(P＜0.05).结论:补充牡蛎低聚肽能够通过改善HPG轴有效防止CTX引起的PADAM的形成,显著改善性功能和生殖功能,并具有一定的剂量效应,以中、高剂量的效果最佳.

摘要： 目的 建立操作简便、重复性好的结直肠癌大鼠热创伤应激模型,用于研究围术期手术应激对肿瘤生长及肿瘤微环境的影响.方法 健康雄性SD大鼠72只,采用随机数字表法分为正常对照组、癌症模型组和热创伤应激组3组,每组24只.癌症模型组和热创伤应激组用N-甲基-N-亚硝基脲(MNU)化学诱导法灌肠16周,建立MNU诱导的结直肠癌模型.16周后热创伤应激组大鼠分别以特制的阻热黄铜模板加热后进行热创伤刺激,并分别于热创伤刺激后0、6、12和24h各随机取6只大鼠取血和采集结直肠组织;正常对照组和癌症模型组也根据热创伤应激组处理时间各随机取6只大鼠取血和采集结直肠组织.采用ELISA法检测大鼠血清促肾上腺皮质激素(ACTH)、IL-6、IL-10、皮质酮水平,采用Western blot法检测结直肠组织细胞周期蛋白(Cyclin) D1和髓样细胞白血病-1(Mcl-1)蛋白水平.结果 热创伤应激组大鼠血清ACTH、IL-6、IL-10、皮质酮水平较正常对照组和癌症模型组均升高,且热创伤应激组创伤应激后6、12、24h血清ACTH、IL-6、IL-10、皮质酮水平较应激后0h均升高,差异均有统计学意义(均P＜0.05).热创伤应激组4个时间点Cyclin D1和Mcl-1蛋白表达水平较正常对照组0h和癌症模型组0h均升高,且热创伤应激组创伤应激后6、12、24h Cyclin D1和Mcl-1蛋白表达水平较应激后0h均升高,差异均有统计学意义(均P＜0.05).结论 结直肠癌大鼠热创伤应激模型具有操作简便、重复性好等优点;热创伤应激可激活IL-6诱导结直肠癌大鼠肿瘤增殖,该模型可用于围术期手术创伤对肿瘤微环境影响的机制研究.

摘要： 背景:研究发现,在脑梗死急性期无论男女均存在不同程度的性激素失衡,在男性则主要表现为睾酮下降、雌二醇升高,随着病情的恢复逐渐趋于正常.目的:探讨雄激素对脑缺血再灌注损伤后脑组织Bcl-2、Bax与Cyt-C表达的影响.方法:120只健康成年雄性SD大鼠由西南医科大学动物实验中心提供,实验方案经西南医科大学动物实验伦理委员会批准(批准号为20170821026).将120只大鼠随机分为假手术组、对照组及低、高剂量雄激素处理组(低剂量组、高剂量组).应用改良Longa法制作大脑中动脉阻断模型大鼠,假手术组不进行插线操作.据脑缺血2 h后再灌注时间点的不同每组再随机分为5个亚组(6,12,24,48,72 h),每亚组5只.24 h时每组另有5只大鼠用于测量脑梗死体积.应用TUNEL法测原位凋亡细胞,免疫组织化学法检测Bcl-2、Bax与Cyt-C的表达情况.结果与结论:①假手术组未见梗死灶,原位凋亡细胞及Bcl-2、Bax与Cyt-C的表达较少,且无动态变化;与对照组相比,低剂量组脑梗死体积百分率、凋亡细胞及Bax与Cyt-C的表达减少,Bcl-2表达增多(均P<0.05),高剂量组则相反(均P<0.05);②除假手术组外,其他3组Bcl-2与Bax于脑缺血再灌注损伤后6 h表达逐渐增强,并于24 h达到高峰,随后逐渐下降;③结果说明,脑缺血再灌注损伤后,低剂量雄激素可能通过减少Bax与Cyt-C的表达、增强Bcl-2的表达,进而减少细胞凋亡,发挥神经保护作用,高剂量则作用相反.

摘要： 目的·观察青春期氰戊菊酯暴露对雄性大鼠睾丸组织氧化应激的影响.方法·将50只Sprague-Dawley (SD)雄性大鼠随机分为对照(玉米油)组、低剂量(0.02 mg/kg氰戊菊酯)组、中剂量(1 mg/kg氰戊菊酯)组、高剂量(50 mg/kg氰戊菊酯)组及干预(50 mg/kg氰戊菊酯+100mg/kg N-乙酰基-L-半胱氨酸)组,每组10只,于4周龄开始连续染毒2个月.测定睾丸组织中丙二醛(malondialdehyde,MDA)含量、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)和超氧化物歧化酶(superoxide dismutase,SOD)活力,并观察大鼠睾丸组织形态结构.结果·与对照组相比,高剂量组大鼠睾丸组织中MDA含量升高,体质量、GSH-Px和SOD活力均下降(均P＜0.05);而干预组与高剂量组相比,MDA含量降低,GSH-Px活力升高(均P＜0.05).睾丸组织形态学观察发现,随着染毒剂量的增加,睾丸生精细胞排列疏松,细胞层数减少,曲细精管管腔内径增大.结论·青春期氰戊菊酯暴露可能导致雄性大鼠睾丸组织氧化损伤.%Objective· To study the effects of fenvalerate exposure during puberty on oxidative stress in rat testis.Methods· Fifty male Sprague-Dawley (SD) rats were randomly divided into the control group (corn oil),low dose group (0.02 mg/kg fenvalerate),moderate dose group (1 mg/kg fenvalerate),high dose group (50 mg/kg fenvalerate) and intervention group (50 mg/kg fenvalerate+100 mg/kg N-acetyl-L-cysteine),ten rats for each group,for two months by gavage at four weeks of age.Malondialdehyde (MDA) content,activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in testis and testicular tissue morphology were detected.Results· Compared with the control group,the rat body weight and activities of GSH-Px and SOD in testis were significantly decreased in high dose group while MDA content was increased (all P＜0.05).Compared with the high dose group,MDA content was decreased and GSH-Px activity was increased in the intervention group (both P＜0.05).The results of testicular histology showed that with the increasing exposure dose,the spermatogenic cells were arranged loosely,the number of layers was decreased and the inner diameter of seminiferous tubules was increased.Conclusion· Exposure to fenvalerate during puberty may induce oxidative damage in testis tissue of male rats.

摘要： 通过全氟辛烷磺酸(perfluomoctane sultanate,PFOS)大鼠灌胃染毒实验评价PFOS对肝功能的影响,探讨PFOS肝毒性反应的潜在机制与可能途径.将Sprague Dawley(SD)雄性大鼠随机分为3组,分别以0 mg·kg-1、5 mg·kg-1和10 mg·kg-1PFOS灌胃染毒28 d.以HE和油红染色法观察大鼠肝脏形态改变.ELISA法测定各组谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate transaminase,AST)、碱性磷酸酶(alkaline phosphatase,ALP)含量变化.化学比色法测定肝匀浆脂代谢水平和氧化产物含量.RT-PCR法检测肝脏内氧化应激以及脂代谢相关基因表达水平.结果表明,PFOS暴露大鼠体重显著降低而肝脏系数显著增加(P＜0.05),与对照组相比PFOS组血清肝功能酶均出现随PFOS浓度增加而升高(P＜0.05).同时大鼠肝脏谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-px)和丙二醛(malondialdehyde,MDA)水平在高剂量组显著升高(P＜0.05),超氧化物歧化酶(superoxide dismutase,SOD)含量先显著升高(P＜0.05)后显著降低(P＜0.05).且肝脏中脂代谢水平也随PFOS浓度的增加而出现显著改变(P＜0.05).PFOS组基因表达均较对照组显著上升(P＜0.05).以上结果说明PFOS具有明显的肝毒性作用,可影响肝脂代谢水平,这可能与PFOS引起的氧化应激所导致的损伤有关.%In order to reveal the toxic effect of perfluorooctane sulphonic acid (PFOS) on SD male rats, the potential mechanisms and possible pathways of PFOS hepatotoxicity were investigated in this study. 30 male SD rats were randomly divided into three groups and 0, 5, 10 mg·kg-1 PFOS were gavaged continuously for 28 days. Morphological changes of the rats liver tissue were examined by HE and Oil red staining. The contents of alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP) in serum were determined by ELISA.The content of triglyceride (TG) and total cholesterol (TC) in the liver was measured by chemical colorimetry. Activity of superoxide dismutase (SOD) was determined by Xanthine oxidase kits and glutathione peroxidase (GSHPx) was determined by DTNB directly. Malondialdehyde (MDA) in SD male rats was measured by Glucosinolates barbituric kits. At the same time, real time fluorescence quantitative PCR was used to detect the levels of gene (Nrf2, NQO1, HO-1, CD36 and SREBP1 c) expression related to oxidative stress and lipid metabolism. The results demonstrated that body weight of rats exposed to 10 mg·kg-1 PFOS showed significant deterioration and the liver coefficient of rats exposed to 5 mg·kg-1 and 10 mg·kg-1 were significantly increased compared with the control in male rats (P＜0.05). Compared with the control, the levels of ALT, ALP and AST increased significantly (P ＜0.05).Furthermore, the GSH-Px activity and MDA content in 10 mg·kg-1 PFOS exposure group and MDA content in 5 mg·kg-1 PFOS exposure group were significantly increased compared with the control in male rats (P ＜ 0.05). While SOD activity was increased significantly in 5 mg·kg-1 PFOS group (P ＜ 0.05) and was reduced significantly in10 mg·kg-1 PFOS group (P ＜ 0.05). In addition, the level of TG in liver was increased while TC was reduced in 5 mg·kg-1 PFOS group and increased significantly in 10 mg·kg-1 PFOS group (P ＜ 0.05). Several genes related to oxidative stress and lipid metabolism such as Nrf2, HO-1, CD36 and SREBP1 c were significantly upregulated in PFOS exposure groups. In conclusion, these results suggest that PFOS has obvious liver toxicity, which may affect the level of liver lipid metabolism. It may be related to the damage caused by PFOS-induced oxidative stress.

摘要： Objective: To study the optimized regimen and antifertility effect of oral administration of low-dose gossypol acetic acid (GA) combined with testosterone undecanoate (TU), desogestral (DSG) and ethinyl estradiol (EE) for contraception in males. Methods: Adult male Wistar rats were randomly divided into 6 groups. Rats in the combined treatment group (LGAH-GA) were administered daily with low-dose of GA (15 mg · kg-1 · d-1 ) plus TU, DSG and EE as loading dose for 7 weeks, followed by a single low-dose GA of 12.5 mg · kg-1 · d-1 from week 8 of treatment for another 17 weeks as a maintenance dose to sustain the infertility. Rat in the combined treatment group (LGAH) were treated with lower-dose of GA (12.5 mg · kg-1 · d-1 ) plus TU, DSG and EE for 7 weeks. Rats in the low-dose gossypol group (LGA) were treated with GA (15 mg · kg-1 · d-1 ) for 24 weeks. Rats in the high-dose gossypol group were treated with GA (30 mg · kg-1 · d-1 ) for 7 weeks. Rats in the hormone group were treated with TU (100 mg · kg-1 · day-1 ,EE and DSG for 14 weeks. Rats in the control group were treated daily with an equal volume of 1% methylcellulose for 24 weeks. Fertility test was used for determining infertility or restoration of fertility in treated rats. Histology examinations were used to examine the alteration on morphology of sperm, testis, epididymides of treated rats. Results: The rats from LGA-A group were completely infertile at week 6 after treatment, and the fulfilled infertility was maintained with single GA (12. 5 mg/kg) only daily after one more week of consolidation treatment with simultaneous administration of low-dose of GA and TU, DSG and EE. Eight weeks after cessation of treatment, all of the treated male rats regained their fertility. The low-dose of GA and TU combined dosage regimen could damage morphology, motility and density of mature sperm, induce infertility within 6 weeks in rats, and rendered treated male rats with spermiation failure within a period of 6-24 weeks of treatment. Conclusion : Oral administration of low dose GA (15 mg · kg-1 · d-1 ) combined with TU, DSG and micro-dose of EE as loading dose could successfully induce infertility in the short term (within 6 weeks). The efficacy could be maintained by a lower dose of GA (12.5 mg · kg 1 · d-1 ) alone in the long term after one extra week of consolidation treatment, and the fertility could recover within a short term after cessation of treatment. The optimized combined regimen provides a promising approach to the development of an effective, reversible, safe and rapid oral male contraceptive.%目的:探索低剂量醋酸棉酚(GA)联合十一酸睾丸酮(TU)、去氧孕烯( DSG)和微量炔雌醇(EE)可逆抗雄性生育作用效果和优化组方.方法:成年雄性Wistar大鼠分为联合用药7周+GA组、联合用药7周组、低剂量GA组、高剂量GA组、激素组和对照组.采用交配试验、组织学形态测定分析法、病理学等方法检测服药雄性大鼠生育能力、附睾精子和睾丸的组织学改变.结果:雄性大鼠联合用药7周+GA组服药6周,不育率达100%,大鼠附睾内长形精子数量减少,90%精子头尾断裂、活力丧失;第8周开始停用激素单独以低剂量GA(12.5 mg·kg-1·d-1)可继续维持抗生育效果17周;停药第8周雄鼠全部恢复生育.结论:口服低剂量GA(15mg· kg-1·d-1为起效剂量,12. 5mg· kg-1·d-1为维持剂量)联合TU (100 mg· kg-1·d-1)、DSG(0.125mg· kg-1·d-1)和微量EE(0. 025 mg·kg-1·d-1),通过严重损伤成熟精子、影响精子形成过程和诱导精子延迟释放发挥避孕效应,抗雄性生育作用起效时间短、效果好、可逆、安全,是优化的低剂量GA联合甾体激素男用避孕药实验用药方案.

摘要： 目的 观察黄芩苷对缺血性脑损伤雄性大鼠的脑保护作用及其对大鼠血清孕酮水平的影响,探讨其可能的作用机制.方法 采用成年SD雄性大鼠制造永久性左侧大脑中动脉梗阻模型,根据神经功能评分,分为模型组、黄芩苷组和抑制剂组,假手术组不插入拴线.造模后于不同时间点进行神经功能评分及双前肢抓力测定,计算抓力下降率;ELISA检测血清孕酮和促肾上腺皮质激素(ACTH)含量.结果 与假手术组比较,模型组大鼠神经功能受损,双前肢抓力显著减小.治疗7 d后,与模型组比较,黄芩苷组神经功能评分降低,双前肢抓力恢复,抓力下降率减小(P<0.05);与黄芩苷组比较,抑制剂组黄芩苷神经功能保护作用降低(P<0.05).治疗7 d后,与模型组比较,黄芩苷组血清孕酮水平显著升高(P<0.01),ACTH水平有升高趋势;与黄芩苷组比较,抑制剂组血清孕酮和ACTH水平均降低(P<0.05).结论 黄芩苷对缺血性脑损伤雄性大鼠的脑保护作用可能与其调控孕酮生成有关.%Objective To investigate the productive effects of baicalin on the male rats with ischemic brain injury and its effects on serum progesterone level in rats; To explore the possible mechanism of baicalin in brain protection. Methods Adult SD male rats were used to create a permanent left middle cerebral artery occlusion model. The rats were evenly divided into model group, baicalin group, inhibitor group, and sham-operation group (without inserted into the intraluminal thread) according to the neurological function scores. At different time points after modeling, the neurological function scores and the grip strength of double foreleg were measured, and the reduction rate of grip strength was calculated. Serum progesterone and adrenocorticotrophic hormone (ACTH) were detected by ELISA. Results Compared with the sham-operation group, the neurological function of rats in the model group was impaired, the grip strength of double foreleg was significantly reduced. 7 days after treatment, compared with the model group, the neurological function score of baicalin group was lowered, grip strength of double foreleg was recovered, reduction rate of grip strength was reduced (P<0.05); compared with the baicalin group, protective effects of baicalin on neurological function was lowered in inhibitor group (P<0.05). 7 days after treatment, compared with the model group, the serum progesterone level in baicalin group was significantly higher (P<0.01), and ACTH level showed an increasing trend; compared with the baicalin group, serum progesterone and ACTH levels in the inhibitor group decreased (P<0.05). Conclusion The protective effects of baicalin on the male rats with ischemic brain injury may be related to the regulation of progesterone.

摘要： 目的：探讨农药氯氰菊酯对对雄性大鼠甲状腺及生殖毒性的影响其剂量-效应关系。rn 方法：用3周龄健康未成熟雄性SD大鼠40只，随机分为对照组(0mg/kg)，氯氰菊酯低、中、高染毒组(18，36，72mg/kg)，每组10只。染毒组以等体积不同浓度花生油稀释配制的氯氰菊酯原药灌胃，灌胃量为0·5ml(次·d)，连续28d；对照组给予等量花生油。第29d清晨麻醉后，心脏采血后，分离睾丸。各指标均采用放免法测定。rn 结果：与阴性对照组相比，血清中T4、T、LH含量随着剂量升高而降低，TSH含量随染毒剂量的增加而增加，差异均有显著性(P<0.05)；各剂量组有明确的剂量-效应关系和线性关系；大鼠睾丸匀浆中ACP、γ-GT和LDH活性在各剂量组均有升高，差异均有显著(P<0.05)。rn 结论：氯氰菊酯对雄性大鼠甲状腺及生殖功能有干扰作用，并引起标志酶活性的变化。

摘要： 环境内分泌干扰物(EEDs)是对维持机体内稳态及调节发育过程有关激素的产生、释放、运转、代谢和清除等生理过程具有影响作用的一类化学物质。迄今已被证实或怀疑具有内分泌干扰作用的化学物质多数具有雌激素的活性。近年来的研究提示雌激素可以影响雄性生殖，敲除雄性大鼠β型雌激素受体(ER-β)基因可造成精子发生障碍：在不同发育时期睾丸的生殖细胞和Settoli细胞中发现ER-β的mRNA及蛋白水平的表达，这说明雌激素在雄性生殖腺中不仅仅是睾酮的代谢产物，同样对精子发生具有密切的关系。rn 本文通过雌激素对雄性大鼠发育阶段的作用，了解雌激素对青春期生殖系统的作用，探讨雌激素对雄性生殖内分泌系统毒性作用特征，为环境内分泌干扰物(类雌激素化学物质)的研究提供阳性基础数据。

摘要： 本发明公开了雄性不育基因ZmTKPR1及其在创制玉米雄性不育系中的应用，ZmTKPR1包括2个旁系同源基因，分别具有SEQ ID NO.1和SEQ ID NO.2所示的核苷酸序列，编码的蛋白质具有SEQ ID NO.3和SEQ ID NO.4所示氨基酸序列。本发明通过CRISPR/Cas9基因编辑技术在野生型玉米中同时定点突变ZmTKPR1的旁系同源基因，创制了tkpr1‑1/2突变体，导致完全雄性不育，发现了ZmTKPR1基因对玉米雄性生殖发育的调控功能。本发明还针对获得的tkpr1‑1/2雄性不育突变体设计了功能分子标记，筛选创制出稳定的玉米雄性不育系，对玉米雄性育性控制和杂交种子生产具有重要意义。

摘要： 本发明公开了雄性不育基因ZmPHD11及其在创制玉米雄性不育系中的应用，具有SEQIDNO.1所示的核苷酸序列，该基因编码的蛋白质具有SEQIDNO.2所示的氨基酸序列。本发明通过CRISPR/Cas9基因编辑技术在野生型玉米中定点突变该基因，可以造成花药发育异常和花粉败育，导致完全的雄性不育，发现了ZmPHD11基因对玉米雄性生殖发育的调控功能。通过后代筛选，可以得到不含转基因成分的不育系，创制出稳定的玉米雄性不育系，对玉米雄性育性控制和杂交种子生产具有重要意义。本发明还针对获得的phd11雄性不育突变体设计了功能分子标记，在玉米雄性不育系培育、不育化杂交制种和分子标记辅助选择中具有重要的应用价值。

摘要： 本发明公开了雄性不育基因ZmMYB33及其在创制玉米雄性不育系中的应用，ZmMYB33包括2个旁系同源基因，分别具有SEQ ID NO.1和SEQ ID NO.2所示的核苷酸序列，编码的蛋白质具有SEQ ID NO.3和SEQ ID NO.4所示的氨基酸序列。本发明通过CRISPR/Cas9基因编辑技术在野生型玉米中同时定点突变ZmMYB33的旁系同源基因，创制了myb33‑1/2突变体，突变体可以导致完全的雄性不育，发现了ZmMYB33基因对玉米雄性生殖发育的调控功能。本发明还针对获得的myb33‑1/2雄性不育突变体设计了功能分子标记，在玉米雄性不育系培育和育化杂交制种具有重要的应用价值。

摘要： 本发明公开了雄性不育基因ZmTGA10及其在创制玉米雄性不育系中的应用，所述基因具有SEQ ID NO.1所示的核苷酸序列，该基因编码的蛋白质具有SEQ ID NO.2所示的氨基酸序列。本发明通过CRISPR/Cas9基因编辑技术在野生型玉米中定点突变该基因，虽然花粉可以正常形成，但花药完全不开裂，发现了ZmTGA10基因对玉米雄性生殖发育的调控功能。通过后代筛选，可以得到不含转基因成分的突变体，创制出稳定的不育系，对研究玉米花药发育具有重要意义。本发明还针对获得的tga10雄性不育突变体设计了功能分子标记，在玉米雄性不育系培育、不育化杂交制种和分子标记辅助选择中具有重要的应用价值。

摘要： 一种提高雄性Wistar大鼠交配能力的方法，属于实验动物生产技术领域，通过采用肉苁蓉、锁阳、淫羊藿和枸杞子四种中药材提取物分别按照0.5mg/mL、1.0 mg/mL、0.6 mg/mL、1.4 mg/mL的浓度配比结合的方式，每日灌胃给雄性Wistar大鼠，使其在短期内交配能力得到明显增强，有效地提高了大鼠捕捉和爬跨次数，显著降低捕捉和爬跨潜伏期，大幅缩短繁殖周期，在实验室鼠类繁育、建立繁殖体系等方面具有成本低、耗时短、操作简单等应用价值，并在濒危哺乳动物繁殖保护、雄性动物勃起功能障碍治疗及开发新药物等方面具有实际的参考依据和广阔的应用前景。

摘要： 本发明提供了一种萝卜胞质雄性不育恢复材料的获得及甘蓝型油菜萝卜胞质雄性不育恢复系的转育方法，该方法包括选用萝卜胞质雄性不特性的瓢儿菜为母本，大规模种植于村庄，在自然状态下与村民种植的萝卜等十字花科蔬菜自由授粉，收获其天然结实种子并种植鉴定，选择其中的可育植株，自由授粉，收获其天然结实种子继续种植，获得萝卜胞质雄性不育恢复材料。第二步利用该萝卜胞质雄性不育恢复材料(可育株)为母本，与优良甘蓝型油菜为父本杂交并连续多代回交、自交，育成甘蓝型油菜萝卜胞质雄性不育恢复系。以该萝卜胞质雄性不育恢复系数为母本，与具有育种目标性状的甘蓝型油菜亲本为父本杂交、回交、自交，选育具有目标性状的甘蓝型油菜恢复系。

摘要： 本发明提供一种介导调控植物隐性核雄性不育系雄性育性的GAT载体及其应用。本发明的GAT载体包括五种功能元件表达盒：植物雄性育性恢复基因元件表达盒，用于恢复隐性核不育突变体的雄性育性；植物花粉败育基因元件表达盒，用于清除含GAT的花粉及保持GAT保持系的杂合状态；化学除草剂正向选择表达盒，用于基因转化及GAT保持系除杂提纯；化学除草剂负向选择表达盒，用于清除除草剂敏感的GAT保持系花粉及种子外逸及GAT不育系除杂提纯；种子筛选元件表达盒，用于种子机械分选。本发明的GAT载体可用于植物隐性核不育材料的杂交育种和杂交制种，从而获得优质高产广适高抗的植物新品种及其种子，具有巨大的经济价值。

摘要： 本发明涉及医用动物培育技术领域，且公开了一种采用复合因子法建立健康SD雄性大鼠肝纤维化方法，包括以下步骤：S1：血干细胞的培养；S2：干细胞活性物的制备；按1：1：1比例将上述A、B和血吸虫血细胞混合，得到血干细胞活性物；S3：将成年SD雄性大鼠进行喂养培养；S4：喂养1周，测定体重后的大鼠开始投喂高脂CDAA饲料，并注射血干细胞活性物；通过将血干细胞、干细胞活性物和血吸虫混合形成复合因子，注射至健康SD雄性大鼠内，这种大鼠制成的动物模型符合NASH向HCC转化的病理过程，易操作、用时短、稳定有效，为研制和开发治疗非酒精性脂肪性肝炎的新药提供造模和技术支持，有巨大的经济和社会效益。

摘要： 本发明公开了一种赶黄草对雄性大鼠正常性功能影响的实验方法，将大鼠随机分为空白对照组，阳性对照15mg/kg万艾可组和赶黄草三个剂量组0.5g生药/kg、1.0g生药/kg、2.0g生药/kg，连续灌胃14d，进行试验，测定赶黄草对大鼠交配能力、性器官重量、阴茎勃起功能、正常雄性大鼠精子的影响。本发明研究结果提示万艾可能提高雄性大鼠的交配能力，但三个剂量赶黄草连续灌胃28天，动物行为活动如常，一般情况良好。实验各组动物交配能力、性器官指数、阴茎勃起功能、精子存活率等无明显促进或抑制作用，与空白对照组比较未见明显差异。因此，赶黄草对雄性大鼠正常性功能无明显影响，长期应用安全。

摘要： 本实用新型公开了一种雄性大鼠睾丸取样分析剖切装置，涉及大鼠手术刀技术领域，该雄性大鼠睾丸取样分析剖切装置，包括刀体和刀柄，所述刀柄的一端设置有夹槽，所述刀体的刀尾插接在夹槽的内部，所述刀体对应刀口的一边设置有切割刃，所述刀体对应刀背的一边设置有挑割刃，且刀体靠近刀尾一端位置的正面和背面均设置有竖直的凸棱，所述刀柄中间段的表面设置有防滑纹和通孔，所述刀柄远离刀体的一端轴线位置设置有尖针。本实用新型通过设置刀柄、夹槽、矩形槽、夹缝、直槽、凸棱、防滑纹、通孔、环形槽和卡环，解决了现有技术中雄性大鼠睾丸取样分析实验使用手术刀的刀片安装比较麻烦容易伤手并且扁平的不锈钢刀柄影响手感的问题。