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目的 探讨表皮生长因子受体 (EGFR)在精子发生过程的作用机制。 方法 ICR雄性小鼠在给予人绒毛膜促性腺激素 (HCG)和切除颌下腺前后采用链霉菌抗生物素蛋白 -过氧化酶 (SP)免疫组织化学结合体视学方法定量分析第 期生精小管上皮的 EGFR阳性静止期精母细胞和各级生精细胞。 结果 与假手术组相比 ,去颌下腺组 EGFR阳性反应静止期精母细胞明显减少 ,同时相应的生精小管的各级生精细胞也显著减少 (P<0 .0 5 )。与去颌下腺组相比 ,去颌下腺给药组和假手术给药组 EGFR阳性反应静止期精母细胞明显增多 ,同时相应的生精小管的生精细胞也显著增多 (P<0 .0 5 )。 结论 静止期精母细胞 EGFR表达减弱是切除颌下腺导致小鼠少精症的原因之一。 HCG可促进静止期精母细胞表达 EGFR,调节精子发生过程
Objective To explore the mechanism of epidermal growth factor receptor (EGFR) in the process of spermatogenesis. Methods ICR male mice were immunostained with streptavidin-peroxidase (SP) immunohistochemistry before and after human chorionic gonadotropin (HCG) and excision of the submandibular gland EGFR positive quiescent spermatocytes and spermatogenic cells at all levels. Results Compared with the sham operation group, the number of spermatocytes in the submandibular gland group at the quiescent phase of EGFR positive was significantly decreased, while the spermatogenic cells at all stages of the corresponding seminiferous tubules were also significantly decreased (P <0.05). Compared with the submandibular gland group, the number of spermatocytes in quiescent phase of EGFR positive reaction in the submandibular gland administration group and the sham operation group was significantly increased, and the number of spermatogenic cells in the corresponding seminiferous tubules was significantly increased (P <0.05) . Conclusions Weak EGFR expression in resting spermatocytes is one of the reasons for oligozoospermia in the submandibular gland. HCG can promote quiescent spermatocytes to express EGFR and regulate the process of spermatogenesis