Disturbance of spermatogenesis and apoptosis
Disturbance of spermatogenesis and apoptosis
批准号:
09470350
负责人:
SASAKI Shoichi
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
项目状态:
已结题
起止时间:
1997 至 1999
中文摘要
精子发生受到各种胁迫的阻碍。有报道称,精子发生失败与细胞凋亡有关。在接下来的各个实验模型中,我们检测了核转录因子-kappaB(NF-κB)在生精障碍中的表达及对细胞凋亡的影响。[围绕1]隐睾症(将成熟大鼠的睾丸固定在腹膜腔内的睾丸高温环境模型大鼠和胎儿期用氟他胺造成的隐睾症大鼠[围绕2]精索扭转(单侧和双侧)[围绕3]精索梗阻(单侧和双侧)[围绕4]化学去势(醋酸亮前列腺素3 mg/kg注射)[围绕5]二乙基已烯雌酚(500μg/体×28天)给药[围绕6]睾丸损伤索(单侧和双侧)睾丸损伤引起的睾丸萎缩更显著的是…在此过程中发现大量凋亡细胞的表达。在单侧[enCircld2]、[enCircld3]和[enCircld6]模型中,对侧被盖也可见细胞凋亡,认为细胞凋亡与自身免疫性炎的危象有关。在[环境2]中,钙依赖的半胱氨酸蛋白酶增加,而抗氧化剂抑制了钙蛋白酶的产生和细胞凋亡的表达。在[环境3]中,一氧化氮合酶的表达随着凋亡细胞的增加而增加。每种模型均观察核转录因子κB向细胞核的转化和P53蛋白的表达与细胞凋亡的关系。此外,在[环绕4]和[环绕5]中给予NFκB抑制因子κB的核内转运,增强细胞的凋亡表达,由此推测,正常大鼠睾丸细胞中的NFκB已被激活,并可能抑制了细胞的凋亡。NF-κ-B活性的抑制可能与生精障碍中细胞凋亡的强烈表达有关。较少
英文摘要
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
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The role of TSP-1 in the pathogenesis of benign prostatic hyperplasia via inflammation.
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批准号:26462451
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$3.16万
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财政年份:2014
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负责人:SASAKI Shoichi
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依托单位:
Exotic hadron-nuclear systems with heavy flavors in lattice QCD
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批准号:23540284
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资助金额:$3.24万
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负责人:SASAKI Shoichi
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依托单位:
Functional analysis of KIT-positeive interstitial cells for novel strategies of molecular target therapies for benign prostatic hyperplasia
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批准号:23592376
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$3.33万
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财政年份:2011
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负责人:SASAKI Shoichi
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依托单位:
Research for signal mechanism of the KIT-positive interstitial cells and development of the new molecular target treatment for the over active bladder
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批准号:20591886
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$3.0万
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财政年份:2008
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负责人:SASAKI Shoichi
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依托单位:
Lattice study of hadron structure and strangness contribution
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批准号:19540265
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.83万
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财政年份:2007
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负责人:SASAKI Shoichi
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依托单位:
Neuropathological study of amyotrophic lateral sclerosis and mutant SOD1 transgenic mice
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批准号:18500280
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.62万
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财政年份:2006
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负责人:SASAKI Shoichi
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依托单位:
Pathological study of mutant SOD1 (G93A and H46R) transgenic mice
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批准号:14570623
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.18万
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财政年份:2002
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负责人:SASAKI Shoichi
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依托单位:
EAAT1 and EAAT2 immunoreactivity in ALS and pathology of SOD1 (G93A) transgenic mice
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批准号:11670646
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.98万
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财政年份:1999
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负责人:SASAKI Shoichi
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依托单位:
Study of the proximal axon of anterior horn neurons in amyotrophic lateral sclerosis
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批准号:01570458
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.34万
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财政年份:1989
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负责人:SASAKI Shoichi
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依托单位:
国内基金
海外基金
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