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基于基因抑制建立少弱精子症小鼠模型。

Establishment of an oligoasthenospermia mouse model based on gene suppression.

机构信息

School of Integrated Traditional Chinese and Western Medicine Anhui University of Chinese Medicine Hefei China.

Anhui Province Key Laboratory of Chinese Medical Formula School of Pharmacy Anhui University of Chinese Medicine Hefei China.

出版信息

Animal Model Exp Med. 2021 Nov 9;4(4):351-358. doi: 10.1002/ame2.12186. eCollection 2021 Dec.

Abstract

BACKGROUND

Oligoasthenospermia is one of the main causes of male infertility. Researchers usually use chemical drugs to directly damage germ cells to prepare oligoasthenospermia models, which disregards the adhesion and migration between spermatogenic cells and Sertoli cells. is a critical regulator of the adhesin of germ cell; thus, we sought to explore a novel oligoasthenospermia model based on gene suppression.

METHODS

Mice in the Pifithrin-α group were injected intraperitoneally with 2.5 mg/kg Pifithrin-α ( inhibitor) daily for 30 consecutive days. Reproductive hormone levels and epididymal sperm quality, as well as the network morphology of Sertoli cells were tested.

RESULTS

Sperm density, motility, and the relative protein and mRNA expression of and were obviously decreased in the Pifithrin-α group compared with the normal control group. No significant distinction was observed in the relative mRNA and protein expression of . Furthermore, the tight junctions (TJs) and apical ectoplasmic specialization (ES) were destroyed in the Pifithrin-α group.

CONCLUSION

The above results indicate that we successfully established a new oligoasthenospermia mouse model. This study provides a foundation for further exploration of the roles of genes during spermatogenesis and provides new research objects for further oligospermia research and future drug discovery.

摘要

背景

少弱精子症是男性不育的主要原因之一。研究人员通常使用化学药物直接损伤精母细胞来制备少弱精子症模型,但这种方法忽略了生精细胞与支持细胞之间的黏附和迁移。 是精子细胞黏附的关键调节因子;因此,我们试图探索一种基于 基因抑制的新型少弱精子症模型。

方法

Pifithrin-α 组小鼠每日腹腔注射 2.5mg/kg Pifithrin-α(抑制剂),连续 30 天。检测生殖激素水平和附睾精子质量,以及支持细胞的网络形态。

结果

与正常对照组相比,Pifithrin-α 组的精子密度、活力以及 和 的相对蛋白和 mRNA 表达明显降低。 基因的相对 mRNA 和蛋白表达无明显差异。此外,Pifithrin-α 组的紧密连接(TJ)和顶外侧质特化(ES)被破坏。

结论

上述结果表明,我们成功建立了一种新的少弱精子症小鼠模型。本研究为进一步探索 基因在精子发生过程中的作用提供了基础,为进一步的少精子症研究和未来的药物发现提供了新的研究对象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9625/8690982/08a363f012e4/AME2-4-351-g001.jpg

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