发育不良小鼠睾丸中细胞周期蛋白 D1/Nanog 和 NF-κB/Bax 蛋白的表达与定位

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY Reproductive toxicology Pub Date : 2024-08-29 DOI:10.1016/j.reprotox.2024.108704
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引用次数: 0

摘要

睾丸发育不良会严重影响男性的生殖能力。本研究采用组织学染色、Western印迹和免疫组织化学方法研究了小鼠发育不良睾丸中细胞周期蛋白D1/Nanog和NF-κB/Bax的表达。结果显示,Nanog和Bax在发育不良睾丸组织中的表达明显高于正常组织(P < 0.01)。正常睾丸组织中 Cyclin D1 蛋白表达高于发育不良睾丸组织(P < 0.01)。NF-κB在隐睾和正常睾丸中高表达,差异无显著性(P > 0.05)。免疫定位显示,Nanog、NF-κB和Bax在Leydig细胞和生精细胞的细胞质中表达。Cyclin D1主要在Sertoli细胞的细胞核中表达。这些发现表明,Nanog、Cyclin D1和Bax的表达改变可能会导致睾丸发育不良。这项研究为检测睾丸发育不良和选择合适的动物模型提供了科学依据,最终为改善男性生殖健康的策略提供信息。
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Expression and localization of Cyclin D1/Nanog and NF-κB/Bax protein in dysplastic testicles of mice

Testicular dysplasia significantly impairs male reproductive capacity. This study investigated the expression of Cyclin D1/Nanog and NF-κB/Bax in dysplastic testes of mice using histological staining, Western blotting, and immunohistochemistry. The results showed that Nanog and Bax expression were significantly higher in dysplastic testicular tissue than in normal tissue (P < 0.01). Cyclin D1 protein expression was higher in normal testis tissue than in dysplastic testis (P < 0.01). NF-κB was highly expressed in cryptorchid and normal testis with no significant difference (P > 0.05). Immunolocalization revealed that Nanog, NF-κB, and Bax were expressed in the cytoplasm of Leydig and spermatogenic cells. Cyclin D1 primarily expressed in the nucleus of Sertoli cells. These findings suggest that altered expression of Nanog, Cyclin D1, and Bax may contribute to testicular dysplasia. This study provides a scientific foundation for detecting testicular dysplasia and selecting appropriate animal models, ultimately informing strategies to improve male reproductive health.

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来源期刊
Reproductive toxicology
Reproductive toxicology 生物-毒理学
CiteScore
6.50
自引率
3.00%
发文量
131
审稿时长
45 days
期刊介绍: Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.
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