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目的研究弓形虫感染对大鼠的雄性生殖损害,探讨其可能的调控机理。方法以2×105/ml速殖子腹腔接种成年雄性SD清洁级大鼠,感染9周,进行大鼠血清性激素、精子数、精子活率、活力、精子质量、睾丸酶活性及睾丸组织的病理学检测。并应用流式细胞仪检测其睾丸组织细胞的凋亡及细胞周期。同时将弓形虫感染雄性组与正常成年雌性SD清洁级大鼠按1∶2合笼交配1周,于妊娠第21天解剖雌性大鼠,检查雌鼠的黄体数、胎鼠的性别、体重、身长和尾长。结果弓形虫感染9周,大鼠的睾丸和附睾的相对重量有所下降,精子数、活力、活率降低,血清性激素水平也降低,睾丸组织也有明显的形态学变化,睾丸组织细胞凋亡率显著高于正常对照组。与弓形虫感染雄性大鼠成功交配的雌性大鼠产仔数显著减少,但胎鼠的平均体重、身长、尾长和胎鼠的性别比例与对照组比较无显著性差异。结论弓形虫感染可诱导大鼠睾丸组织细胞发生凋亡,弓形虫感染对大鼠雄性生殖系统有一定程度的损害,对雄性生育功能也有一定影晌,其进一步的损伤及调控机理尚待更深入的研究。
Objective To study the male reproductive damage of Toxoplasma gondii infection in rats and to explore its possible regulatory mechanism. Methods Adult male SD rats were inoculated intraperitoneally with 2 × 105 / ml tachyzoites for 9 weeks. Serum sex hormones, sperm counts, sperm motility, sperm motility, sperm quality, testicular enzyme activity and testicular tissue pathology Neutrino test. Flow cytometry was used to detect the apoptosis and cell cycle of testicular cells. At the same time, Toxoplasma gondii-infected male group and normal adult female SD clean-grade rats were mated for 1 week with 1: 2 cage. The female rats were dissected on the 21st day of gestation to check the luteal number, sex, weight, Length and tail length. Results Toxoplasma gondii infection for 9 weeks decreased the relative weight of testis and epididymis in rats, decreased the number of sperm, decreased the activity of vitality, reduced the level of serum sex hormones and marked morphological changes of testicular tissue. The apoptosis rate of testicular tissue Significantly higher than the normal control group. The average litter size, body length, tail length and fetal rat sex ratio were not significantly different from those of the control group. The number of littermates in female rats successfully mated with Toxoplasma gondii male rats decreased significantly. Conclusion Toxoplasma gondii infection can induce the apoptosis of testicular cells in rats. Toxoplasma gondii infection can damage the male reproductive system to some extent, and has some influence on male reproductive function. The further damage and regulation mechanisms need to be further studied Research.