Bindoni M, Belluardo N, Marchese A E, Cardile V, Mudò G, Cella S, Laguidara A, Denatale G
Neuroendocrinology. 1986;42(5):407-15. doi: 10.1159/000124479.
A significant increase of cell multiplication in inoculated ascitic and solid tumors was demonstrated in both DBA/2 and C57BL/6 mice as well as in Wistar rats after radiofrequency lesions in the median hypothalamus (ventromedial and dorsomedial nuclei; part of arcuate nucleus). The following tests were performed: mitotic and metaphasic index, doubling time of tumor, incorporation of tritiated thymidine into DNA, cell cycle parameters and growth fraction. The increased rate of cell proliferation measured was predominantly due to the higher speed of DNA biosynthesis with a minor contribution by an increase of the growth fraction. In the animals with hypothalamic lesions we demonstrated a slight decrease in the secretory activity of the adenohypophysis. Because it is generally stated that failure of hypophysis function hinders cell multiplication in normal and neoplastic tissues, we think that heightened cell proliferation after hypothalamic lesions is due to suppression of an inhibitory mechanism located in the hypothalamus and which is independent of the hypophysis.
在DBA/2和C57BL/6小鼠以及Wistar大鼠中,下丘脑正中(腹内侧核和背内侧核;弓状核部分)进行射频损伤后,接种的腹水瘤和实体瘤中的细胞增殖显著增加。进行了以下测试:有丝分裂和中期指数、肿瘤倍增时间、氚标记胸腺嘧啶核苷掺入DNA、细胞周期参数和生长分数。所测得的细胞增殖率增加主要是由于DNA生物合成速度加快,生长分数增加的贡献较小。在有下丘脑损伤的动物中,我们发现腺垂体的分泌活性略有下降。由于一般认为垂体功能衰竭会阻碍正常组织和肿瘤组织中的细胞增殖,我们认为下丘脑损伤后细胞增殖增强是由于下丘脑存在一种与垂体无关的抑制机制受到抑制。