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沙利度胺对费希尔344大鼠雌激素诱导的催乳素瘤生长、分泌功能及血管生成的抑制作用

Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats.

作者信息

Stepień Henryk, Lawnicka Hanna, Mucha Sławomir, Wagrowska-Danilewicz Małgorzata, Stepień Bartłomiej, Siejka Agnieszka, Komorowski Jan

机构信息

Department of Immunoendocrinology, Medical University of Lodz, Dr Sterling 3 Street, 91-425 Lodz, Poland.

出版信息

Life Sci. 2006 Sep 27;79(18):1741-8. doi: 10.1016/j.lfs.2006.06.013. Epub 2006 Jun 15.

Abstract

The process of angiogenesis has been found to be essential for the development of estrogen-induced pituitary prolactinoma in Fischer 344 rats. Thalidomide [(alpha-(N-phthalimido)-glutarimide] is known to be a potent immunomodulatory drug with antiangiogenic properties, but its effect on lactotroph cell secretory function and pituitary prolactinoma formation has not been described yet. The purpose of this study was to examine the effects of thalidomide on secretion of prolactin (PRL) and vascular endothelial growth factor (VEGF), cell proliferation, apoptosis and angiogenesis within the anterior pituitary gland in long-term diethylstilboestrol (DES)-treated male F344 rats in vivo and in vitro. It was found that DES sharply increased serum PRL and VEGF levels. On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion. It also diminished prolactin cell proliferation evaluated as the number of proliferating cell nuclear antigen (PCNA)-positive stained cell nuclei and increased the number of apoptotic bodies determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the DES-induced pituitary prolactinoma. The density of pituitary microvessels evaluated by microscopic counting of CD-31-positive blood vessels was also diminished by the tested drug. In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro. In conclusion, our results provide strong evidence for the antiprolactin and antitumor activity of thalidomide in experimentally DES-induced pituitary adenoma.

摘要

血管生成过程已被发现对于费希尔344大鼠中雌激素诱导的垂体催乳素瘤的发展至关重要。沙利度胺[α-(N-邻苯二甲酰亚胺基)-戊二酰亚胺]是一种具有抗血管生成特性的强效免疫调节药物,但其对催乳素细胞分泌功能和垂体催乳素瘤形成的影响尚未见报道。本研究的目的是在体内和体外研究沙利度胺对长期接受己烯雌酚(DES)处理的雄性F344大鼠垂体前叶催乳素(PRL)和血管内皮生长因子(VEGF)分泌、细胞增殖、凋亡及血管生成的影响。结果发现,DES显著提高血清PRL和VEGF水平。另一方面,在实验的最后15天对F344大鼠同时给予沙利度胺治疗,减弱了DES对PRL和VEGF分泌的刺激作用。它还减少了以增殖细胞核抗原(PCNA)阳性染色细胞核数量评估的催乳素细胞增殖,并增加了通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)法在DES诱导的垂体催乳素瘤切片中测定的凋亡小体数量。通过显微镜计数CD-31阳性血管评估的垂体微血管密度也因受试药物而降低。此外,沙利度胺(10^(-4)至10^(-6) M)抑制体外培养的大鼠垂体催乳素瘤细胞的增殖、催乳素和VEGF分泌。总之,我们的结果为沙利度胺在实验性DES诱导的垂体腺瘤中的抗催乳素和抗肿瘤活性提供了有力证据。

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