论文部分内容阅读
为了探讨人绒毛膜促性腺激素 (h CG)与颌下腺、睾丸和附睾表皮生长因子(EGF)的相互调节机制 ,本研究对 ICR雄性小鼠在切除颌下腺和给予 h CG前后应用放射免疫方法测定睾丸和附睾 EGF变化以及睾丸和血清睾酮 (T)变化。结果 :去颌下腺后 ,睾丸 EGF和血清 T不降低 (P>0 .0 5 ) ,附睾 EGF明显增加 (P<0 .0 5 ) ,睾丸 T显著降低(P<0 .0 5 ) ;去颌下腺给药组与去颌下腺组相比 ,睾丸和附睾 EGF明显增加 (P<0 .0 5 ) ,睾丸 T明显增加 (P<0 .0 5 ) ,血清 T显著降低 (P<0 .0 5 )。假手术给药组与假手术组相比 ,睾丸和附睾 EGF明显增加 (P<0 .0 5 ) ,睾丸 T明显增高 (P<0 .0 5 ) ,血清 T不增加 (P<0 .0 5 )。假手术给药组与去颌下腺给药组相比 ,睾丸 EGF明显增加 (P<0 .0 5 ) ,附睾EGF明显降低 (P<0 .0 5 ) ,睾丸 T和血清 T均明显增加 (P<0 .0 5 )。结论 :(1 )睾丸与附睾均能产生 EGF。 (2 ) h CG可通过调节睾丸 T生物合成影响睾丸、附睾 EGF含量。 (3)颌下腺促进睾丸 T的生物合成。 (4 )颌下腺和 h CG调节睾丸、附睾 EGF合成的机制不同。
In order to investigate the mechanism of human chorionic gonadotropin (hCG) and submandibular gland, testis and epididymal epidermal growth factor (EGF) mutual regulation, the study of ICR male mice before and after resection of the submandibular gland and given CGG radioimmunoassay method testis And epididymal EGF changes and testis and serum testosterone (T) changes. Results: After going to the submandibular gland, testicular EGF and serum T did not decrease (P> 0.05), epididymal EGF increased significantly (P <0.05), testicular T decreased significantly (P <0.05) Compared with the submandibular gland group, the testis and epididymis significantly increased (P <0.05), the testicular T increased significantly (P <0.05) . Compared with the sham-operation group, the testis and epididymis significantly increased (P <0.05), the testicular T increased significantly (P <0.05) and the serum T did not increase (P <0. 0) 5). Compared with the submandibular gland administration group, the testicular EGF significantly increased (P <0.05), the epididymal EGF decreased significantly (P <0.05), the testicular T and serum T significantly increased (P <0 .0 5). Conclusion: (1) Both testis and epididymis can produce EGF. (2) h CG can affect testis, epididymis EGF content by regulating testicular T biosynthesis. (3) Submandibular gland promote testicular T biosynthesis. (4) submandibular gland and h CG regulate testis, epididymis EGF synthesis mechanism is different.