Abstract

Genetic defects during spermatogenesis can lead to a reduction in sperm motility and cause male infertility. The cation channels of sperm (CatSper) play a role in the regulation of hyperactivated sperm motility in mouse testes. The effect of Trigonellae Semen (TS) on the male reproductive system and CatSper protein in mouse testes during spermatogenesis was examined. C57BL/c mice were divided into the following five groups: normal, cyclophosphamide- (CP-) only treated (control group), and three groups treated with varying concentrations of TS with CP (100, 500, and 1000 mg/kg TS and 100 mg/kg CP). Real-time PCR, western blot analysis, and a testosterone immunoassay were performed to assess CatSper protein levels in the five groups. Additionally, sperm cell counts and motility were examined. Results indicate that sperm motility and sperm counts increased in the TS treated groups in a dose-dependent manner (p < 0.01). CatSper levels were also significantly higher in the TS treated groups compared to that of the control group (p < 0.001). Therefore, TS treatment could enhance sperm function by promoting spermatogenesis and the expression of CatSper proteins in mouse testes.

Highlights

  • Spermatogenesis is a complex process of male germ cell proliferation, differentiation, and maturation from diploid spermatogonia to haploid spermatozoa in the seminiferous tubules of the testes [1]

  • This study investigated the effects of the Trigonellae Semen (TS) extract on spermatogenesis and CatSper gene expression in mice using cyclophosphamide (CP) to induce testicular toxicity

  • Sperm cell motility in the CP and TS groups (100, 500, and 1000 mg/kg) was greater than that in the control group (17.56 ± 8.24, 24.41 ± 6.69, and 16.49 ± 6.75%, resp.; p < 0.05, Figure 1(b)). Sperm velocity parameters such as average path velocity (VAP, μm/s), straight line velocity (VSL, μm/s), curvilinear velocity (VCL, μm/s), and amplitude of lateral head displacement (ALH) of control group have significantly decreased compared to normal group

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Summary

Introduction

Spermatogenesis is a complex process of male germ cell proliferation, differentiation, and maturation from diploid spermatogonia to haploid spermatozoa in the seminiferous tubules of the testes [1]. The biological process of sperm production is regulated hormonally through feedback mechanisms using Leydig cells to promote testosterone production and cell signaling such as a Sertoli and Leydig cell [2]. This paracrine and endocrine regulation of germ cell development requires spermatogenic stage- and cell-specific gene expression [3]. It has been estimated that over 2000 proteins are involved in the specialized regulation of spermatogenesis [4, 5] Genetic disorders such as chromosomal abnormalities or single gene mutations can impair spermatogenesis or reduce sperm cell function and can result in male infertility [5,6,7,8]. It is necessary to investigate the effects of controlled drugs for testis-specific gene expression or identify novel genetic biomarkers of normal spermatogenesis

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