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首页> 外文期刊>Life sciences >Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats.
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Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats.

机译：沙利度胺对Fischer 344大鼠雌激素诱导的催乳素瘤的生长，分泌功能和血管生成的抑制作用。

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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.
机译：已发现在Fischer 344大鼠中，血管生成过程对于雌激素诱导的垂体泌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）]是一种有效的具有抗血管生成特性的免疫调节药物，但尚未描述其对泌乳营养细胞分泌功能和垂体泌乳素瘤形成的作用。在体内和体外研究了沙利度胺对长期二乙基雌二醇（DES）处理的雄性F344大鼠泌乳素（PRL）和血管内皮生长因子（VEGF）分泌，垂体前腺内细胞增殖，凋亡和血管生成的影响发现DES可以显着增加血清PRL和VEGF的含量;另一方面，在实验的最后15天同时用沙利度胺同时治疗F344大鼠，减弱了DES对PRL和VEGF分泌的刺激作用，也减少了催乳素。细胞增殖评估为增殖细胞核抗原（PCNA）阳性染色的细胞核数目，并增加凋亡小体数目在DES诱导的垂体泌乳素瘤的部分中，通过末端脱氧核苷酸介导的dUTP缺口末端标记（TUNEL）方法进行了检测。通过显微镜计数CD-31阳性血管评估的垂体微血管的密度也被测试药物降低。此外，沙利度胺（10（-4）至10（-6）M）抑制体外培养的大鼠垂体泌乳素瘤细胞的细胞增殖，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的证据。

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