Pendrin and sodium/iodide symporter protein expression in the testicular tissue of normal and diabetic rats in prepubertal and post pubertal stages

青春期前和青春期后正常和糖尿病大鼠睾丸组织中 Pendrin 和钠/碘转运蛋白的表达

阅读:24
作者:T Karaca, S Demirtas, D Uzun Goren

Abstract

Pendrin (PDS) and sodium/iodide symporter (NIS) are transmembrane proteins that are located in numerous tissue types, particularly thyroid follicular epithelial cells, where they are entrusted with the regulation of iodine molecules. In the present study, we aimed to clarify changes in PDS and NIS protein expression, in the testicular tissue of prepubertal and post pubertal rats at normal or diabetic conditions. Forty Wistar albino male rats (20 prepubertal and 20 post pubertal) were divided into four groups, as follows: group I was prepubertal control, group II was prepubertal diabetic (60 mg/kg intraperitoneal [ip] streptozotocin [STZ]), group III was post pubertal control, and group IV was post pubertal diabetic (60 mg/kg ip STZ). Ki67 immunoreactivity decreased in testicular tissue of both the prepubertal and post pubertal diabetic groups; the apoptotic tubule index and apoptotic cell number increased in the diabetic groups as compared to the control groups. Pendrin immunoreactivity was detected in seminiferous tubules and Leydig cells; and was significantly reduced in the diabetic groups (P<0.05). The number of cells positive for NIS was significantly decreased in prepubertal and post pubertal rats with diabetes, compared to the controls. Enzyme-linked immunosorbent assay (ELISA) analysis showed that PDS and NIS values were significantly reduced in the prepubertal and post pubertal diabetic groups as compared to the control groups. Our results indicate a potential relationship between puberty and PDS and NIS expression in rat testicular tissue and showed the decreasing effects of diabetes on PDS and NIS expression in testicular tissues in rats.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。