Okada M, Sato E, Miyamoto H, Toyoda Y
Department of Reproductive and Developmental Biology, University of Tokyo, Japan.
Endocr J. 1995 Oct;42(5):675-81. doi: 10.1507/endocrj.42.675.
HPLC-purified glycosaminoglycans (hpGAG) prepared from extracts of non-luteal mouse (JcL:ICR strain) ovaries were assayed for neovascularization by implanting Elvax films, containing test samples, on the lateral wall of the sheath of m. rectus abdominis in adult female mice of the same strain. Neovascularization occurred in a dose-dependent manner, and was characterized by capillary outgrowth extending into the tissue surrounding the implant. The single major peak of purified GAG on a column of TSK gel DEAE got out of order after treatment with streptococcal hyaluronidase or nitrous acid. The activity of this fraction was also greatly reduced when treated with streptococcal hyaluronidase or nitrous acid. When hpGAG was embedded in the implant with 17 alpha-hydroxyprogesterone at a dose of 20 micrograms/film, neovascularization induced by means of hpGAGs was suppressed. Progesterone at a dose of 50 micrograms/film did not suppress the neovascularization induced by ovarian hpGAG. These findings suggest that 17 alpha-hydroxyprogesterone suppresses the angiogenic activity of hyaluronic acid-like hpGAG in the ovary.
从非黄体期小鼠(JcL:ICR品系)卵巢提取物中制备的高效液相色谱纯化糖胺聚糖(hpGAG),通过将含有测试样品的埃尔瓦克斯膜植入同品系成年雌性小鼠腹直肌鞘侧壁来检测其促血管生成作用。血管生成呈剂量依赖性,其特征是毛细血管延伸至植入物周围组织。经链球菌透明质酸酶或亚硝酸处理后,TSK凝胶DEAE柱上纯化GAG的单一主峰出现紊乱。用链球菌透明质酸酶或亚硝酸处理后,该组分的活性也大大降低。当hpGAG与17α-羟基孕酮以20微克/膜的剂量包埋在植入物中时,hpGAG诱导的血管生成受到抑制。50微克/膜剂量的孕酮并未抑制卵巢hpGAG诱导的血管生成。这些发现表明,17α-羟基孕酮可抑制卵巢中类似透明质酸的hpGAG的血管生成活性。