Cheuk B L, Leung P S, Lo A C, Wong P Y
Department of Physiology, The Chinese University of Hong Kong, Shatin, N.T, Hong Kong.
Biol Reprod. 2000 Sep;63(3):775-80. doi: 10.1093/biolreprod/63.3.775.
Bradykinin and a number of peptide hormones such as angiotensin, endothelin, and vasopressin stimulate anion secretion in rat epididymis via local formation of PGE(2). These effects are mediated by cyclooxygenase (COX)-1 isozyme. The present study was undertaken to assess the androgen control of COX expression in the epididymis. Adult male Sprague-Dawley rats were bilaterally castrated through a scrotal route. Reverse transcription-polymerase chain reaction was used to measure COX-1 and COX-2 mRNAs in the epididymis in normal and castrated rats. Anion secretion in epithelia grown from the epididymides of these rats was studied by the short-circuit current technique. In normal rats, COX-1 and COX-2 mRNAs were detected in the intact epididymis. Elimination of spermatozoa by the technique of efferent duct ligation or flushing out spermatozoa did not affect the expression of either enzyme in the epididymis, indicating that the epithelium, but not spermatozoa, expressed the enzymes. Castration caused a time-dependent decrease in expression of COX-1 and COX-2 mRNAs, which were partially restored upon testosterone replacement. In epithelia cultured from castrated rats, there was a complete loss of bradykinin-induced anion secretion. This effect was reversible upon testosterone replacement. Although epithelia from castrated rats did not respond to bradykinin, they could respond to cAMP, forskolin, and PGE(2) with only 20% loss of response magnitude when compared with epithelia from normal rats. These results suggest that the expression of COX-1 and COX-2 are dependent on androgen. The loss of COX-1 expression after castration correlates with the specific loss of anion secretion induced by bradykinin and possibly other hormones.
缓激肽以及一些肽类激素，如血管紧张素、内皮素和血管加压素，通过局部生成前列腺素E2（PGE2）刺激大鼠附睾中的阴离子分泌。这些作用由环氧化酶（COX）-1同工酶介导。本研究旨在评估雄激素对附睾中COX表达的调控。成年雄性Sprague-Dawley大鼠通过阴囊途径进行双侧去势。采用逆转录聚合酶链反应来测量正常和去势大鼠附睾中COX-1和COX-2的信使核糖核酸（mRNA）。通过短路电流技术研究这些大鼠附睾上皮细胞的阴离子分泌。在正常大鼠中，完整的附睾中可检测到COX-1和COX-2的mRNA。通过输出小管结扎技术去除精子或冲洗出精子并不影响附睾中这两种酶的表达，表明是上皮细胞而非精子表达这些酶。去势导致COX-1和COX-2 mRNA的表达随时间下降，睾酮替代后部分恢复。在去势大鼠培养的上皮细胞中，缓激肽诱导的阴离子分泌完全丧失。这种作用在睾酮替代后是可逆的。尽管去势大鼠的上皮细胞对缓激肽无反应，但与正常大鼠的上皮细胞相比，它们对环磷酸腺苷（cAMP）、福斯可林和PGE2仍有反应，反应幅度仅降低20%。这些结果表明，COX-1和COX-2的表达依赖于雄激素。去势后COX-1表达的丧失与缓激肽及可能其他激素诱导的阴离子分泌的特异性丧失相关。
