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目的:利用邻苯二甲酸二丁酯(DBP)诱导大鼠睾丸发育异常,验证泛素碳端水解酶L1(UCHL1)在异常睾丸与正常大鼠睾丸中的差异表达,以进一步探讨UCHL1在DBP导致的大鼠睾丸发育异常中的作用机制。方法:孕SD大鼠40只,妊娠14~18d,随机分为2组,实验组和对照组分别予DBP 800mg/(kg·d)、大豆油5ml/d灌胃,孕期第19d(GD19)和出生后22d(PND22),分别取胎鼠及仔鼠睾丸,定量定位分析UCHL1在胎鼠及仔鼠睾丸中的表达变化。结果:GD19,UCHL1在实验组的相对表达量为0.075±0.02(n=10),对照组为0.150±0.02(n=10),2组差异有显著性(P<0.05),UCHL1在实验组中比正常对照组下降50%;而PND22,UCHL1于实验组隐睾睾丸中的相对表达量为0.344±0.03(n=10),实验组非隐睾睾丸中为0.326±0.02(n=10),对照组为0.322±0.02(n=10),3组间无明显统计学差异(P>0.05)。UCHL1主要定位于睾丸发育时期的精原细胞,初级精母细胞和次级精母细胞的胞质与胞核中。结论:DBP在染毒期间影响了睾丸生精细胞UCHL1的表达,影响了泛素-蛋白酶体系的平衡,从而导致生精小管的变薄,各层生精细胞数目减少的睾丸发育异常现象。
OBJECTIVE: To investigate the differential expression of UCHL1 in testis of abnormal testes and normal rats by using DBP induced testicular dysplasia in rats, and to further explore the role of UCHL1 in DBP Induced rat testicular dysplasia in the mechanism of action. Methods: Forty pregnant SD rats were randomly divided into two groups at 14-18 days of gestation. The experimental group and the control group were given DBP 800mg / (kg · d), soybean oil 5ml / And postnatal day 22 (PND22). Fetal and offspring testes were taken respectively and the expression of UCHL1 in fetal testes and offspring testes was quantitatively analyzed. Results: The relative expression levels of GD19 and UCHL1 in the experimental group were 0.075 ± 0.02 (n = 10) and 0.150 ± 0.02 (n = 10) in the control group, with significant difference between the two groups (P <0.05) (N = 10). The relative expression of PND22 and UCHL1 in testis of cryptorchid testis was 0.344 ± 0.03 (n = 10) in test group and 0.326 ± 0.02 (n = 10) in non-cryptorchid testis in experimental group , And the control group was 0.322 ± 0.02 (n = 10). There was no significant difference between the three groups (P> 0.05). UCHL1 is mainly located in the cytoplasm and nucleus of spermatogonia, primary spermatocytes and secondary spermatocytes during testicular development. CONCLUSION: DBP affects the expression of UCHL1 in testicular germ cells during exposure and affects the balance of ubiquitin-protease system, resulting in the thinning of seminiferous tubules and the abnormal development of testis with reduced number of spermatogenic cells in each layer.