Disturbance of spermatogenesis and apoptosis

精子发生和细胞凋亡的干扰

基本信息

  • 批准号:
    09470350
  • 负责人:
  • 金额:
    $ 7.3万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 财政年份:
    1997
  • 资助国家:
    日本
  • 起止时间:
    1997 至 1999
  • 项目状态:
    已结题

项目摘要

The spermatogenesis is hindered by various stresses. It is reported that the apoptosis is concerned in the spermatogenesis failure. Using the rat in each following experimental model, we examined the expression of the apoptosis and involvement of transcription factor nuclear factor-kappa B(NFκB) for the disorder of spermatogenesis. 【encircled1】 cryptorchidism (model rat of high temperature environment of testicles which fixed the testicles of the maturation rat in the peritoneal cavity and cryptorchidism rat made by administering Flutamide for the fetal stage 【encircled2】 torsion of thespermatic cord (unilateral and bilateral) 【encircled3】 the obstruction of seminal tract cord (unilateral and bilateral) 【encircled4】 the chemical castration (leuprolerin acetate 3mg/kg administration) 【encircled5】 diethylstilbesterol (500μg/body x 28days) administration 【encircled6】 testicular trauma cord (unilateral and bilateral)The testes of either model caused the atrophy of which was more significan … More t than the controls, and the expression of large number of apoptotic cells was recognized in the process. In the unilateral model of 【encircled2】,【encircled3】 and 【encircled6】, the apoptosis was also recognized in the contra-lateral tedticles, and it considered that the apoptosis was related with the crisis of the autoimmune orchitis. In 【encircled2】 the calpain which was the calcium-dependent cysteine protease increased, and calpain production and apoptosis expression were suppressed by the antioxidant. In 【encircled3】 the expression of the NOS increased with the increase in the apoptosis cell. In each model the conversion of NFκB to the nucleus and the expression of the p53 protein were observed with the apoptosis expression. In addition, the nucleus internal transportation of NFκB was suppressed, and the apoptosis expression was strengthened when the inhibitor of NFκB was administered in 【encircled4】 and 【encircled5】.From the above results, it was considered that NFκB had been activated in the normal rat testicular cells, and it might suppress the apoptosis. The suppression of the NFκB activity seemed to be concerned in the strong expression of the apoptosis in the disturbance of the spermatogenesis. Less
精子发生受到各种应激的阻碍。研究表明,细胞凋亡与精子发生障碍有关。采用以下各实验模型,检测睾丸细胞凋亡的表达及转录因子核因子-κ B(NFκB)在精子发生障碍中的作用。隐睾症(睾丸高温环境模型大鼠,将成熟大鼠的睾丸固定在腹腔内,隐睾大鼠通过给药氟啶用于胎儿期[包围2]精索扭转(单侧和双侧)[包围3]精道索阻塞(单侧和双侧)[圈4]化学阉割(醋酸亮丙瑞林3 mg/kg给药)[圈环5]己烯雌酚(500μg/体× 28天)给药[圈6]睾丸创伤索(单侧和双侧)两种模型的睾丸均引起萎缩, ...更多信息 与对照组相比,在此过程中发现了大量凋亡细胞的表达。在[encircled 2]、[encircled 3]和[encircled 6]的单侧模型中,对侧睾丸组织中也发现了凋亡,认为凋亡与自身免疫性睾丸炎的危象有关。在[encircled 2]中,钙依赖性半胱氨酸蛋白酶钙蛋白酶增加,抗氧化剂抑制钙蛋白酶的产生和凋亡表达。在[encircled 3]中,NOS的表达随着凋亡细胞的增加而增加。在各模型中观察NFκB B向核内的转化和p53蛋白的表达及细胞凋亡的表达。此外,在[encircled 4]和[encircled 5]中给予NFκB抑制剂后,NF κ B的核内转运受到抑制,凋亡表达增强,上述结果表明正常大鼠睾丸细胞中NFκB已被激活,可能抑制了凋亡。NFκB活性的抑制可能与精子发生障碍时细胞凋亡的强烈表达有关。少

项目成果

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SASAKI Shoichi其他文献

SASAKI Shoichi的其他文献

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{{ truncateString('SASAKI Shoichi', 18)}}的其他基金

The role of TSP-1 in the pathogenesis of benign prostatic hyperplasia via inflammation.
TSP-1 通过炎症在良性前列腺增生发病机制中的作用。
  • 批准号:
    26462451
  • 财政年份:
    2014
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Exotic hadron-nuclear systems with heavy flavors in lattice QCD
晶格 QCD 中具有浓郁风味的奇异强子核系统
  • 批准号:
    23540284
  • 财政年份:
    2011
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Functional analysis of KIT-positeive interstitial cells for novel strategies of molecular target therapies for benign prostatic hyperplasia
KIT阳性间质细胞的功能分析用于良性前列腺增生分子靶向治疗新策略
  • 批准号:
    23592376
  • 财政年份:
    2011
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Research for signal mechanism of the KIT-positive interstitial cells and development of the new molecular target treatment for the over active bladder
KIT阳性间质细胞信号机制研究及膀胱过度活动症新型分子靶向治疗药物开发
  • 批准号:
    20591886
  • 财政年份:
    2008
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Lattice study of hadron structure and strangness contribution
强子结构和奇异性贡献的晶格研究
  • 批准号:
    19540265
  • 财政年份:
    2007
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Neuropathological study of amyotrophic lateral sclerosis and mutant SOD1 transgenic mice
肌萎缩侧索硬化症和突变SOD1转基因小鼠的神经病理学研究
  • 批准号:
    18500280
  • 财政年份:
    2006
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Pathological study of mutant SOD1 (G93A and H46R) transgenic mice
突变型SOD1(G93A和H46R)转基因小鼠的病理研究
  • 批准号:
    14570623
  • 财政年份:
    2002
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
EAAT1 and EAAT2 immunoreactivity in ALS and pathology of SOD1 (G93A) transgenic mice
ALS 中的 EAAT1 和 EAAT2 免疫反应性以及 SOD1 (G93A) 转基因小鼠的病理学
  • 批准号:
    11670646
  • 财政年份:
    1999
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Study of the proximal axon of anterior horn neurons in amyotrophic lateral sclerosis
肌萎缩侧索硬化症前角神经元近端轴突的研究
  • 批准号:
    01570458
  • 财政年份:
    1989
  • 资助金额:
    $ 7.3万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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