Suzuki H, Nakada T
Department of Urology, Yamagata University School of Medicine, Japan.
Arch Androl. 1996 May-Jun;36(3):205-16. doi: 10.3109/01485019608987097.
Two series of experiments were conducted to clarify the collagen biosynthesis and isolation of type I and type III collagens of young rats that received various sex hormone treatments. Evidence has been presented that (1) estradiol-17 beta treatment induces prostatic atrophy and suppresses the incorporation of [3H]proline into collagen in prostate; (2) administration of estradiol-17 beta increases the collagen content in the prostate; (3) localization of type I and III collagens in the interstitium of the prostate is detected by indirect immunofluorescence staining; (4) the ratio of type III collagen to type I collagen in the gland decreases following estradiol-17 beta treatment; and (5) neither treatment with testosterone nor administration of testosterone plus estradiol-17 beta in precastrated rats shows discernible effects on these valuables. These findings suggest that estradiol-17 beta increases the accumulation of collagen into the prostate with different extents of influence on the synthesis of type I and III collagens.
进行了两组实验,以阐明接受不同性激素处理的幼鼠I型和III型胶原蛋白的生物合成及分离情况。已有证据表明:(1)17β-雌二醇处理会导致前列腺萎缩,并抑制[3H]脯氨酸掺入前列腺胶原蛋白中;(2)给予17β-雌二醇会增加前列腺中的胶原蛋白含量;(3)通过间接免疫荧光染色检测到I型和III型胶原蛋白在前列腺间质中的定位;(4)17β-雌二醇处理后,腺体中III型胶原蛋白与I型胶原蛋白的比例降低;(5)在去势大鼠中,单独给予睾酮或睾酮加17β-雌二醇处理对这些指标均无明显影响。这些发现表明,17β-雌二醇增加了胶原蛋白在前列腺中的积累,且对I型和III型胶原蛋白的合成有不同程度的影响。