Kitajima Yoshimitsu, Endo Toshiaki, Manase Kengo, Nishikawa Akira, Shibuya Masabumi, Kudo Ryuichi
Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, South 1 West 16, Chuo-ku, Sapporo 060-8543, Japan.
Fertil Steril. 2004 Mar;81 Suppl 1:842-9. doi: 10.1016/j.fertnstert.2003.11.012.
Using hyperstimulated rats, to elucidate the mechanisms of gonadotropin-releasing hormone agonist (GnRH-a) treatment to prevent early ovarian hyperstimulation syndrome (OHSS).
Descriptive study of hyperstimulated rats as an early OHSS model with Western blot analysis, Northern blot hybridization, and vascular permeability assay.
Experimental laboratory research.
ANIMAL(S): Sprague-Dawley female rats were used for collecting ovarian samples.
INTERVENTION(S): Hyperstimulated rats received consecutive GnRH-a treatment from the start of pregnant mare serum gonadotropin (PMSG) treatment through 2 days after hCG administration.
MAIN OUTCOME MEASURE(S): Expressions of vascular endothelial growth factor (VEGF), VEGF receptor-1 (VEGFR-1: Flt-1), VEGF receptor-2 (VEGFR-2: KDR/Flk-1), and vascular permeability by Evans blue leakage.
RESULT(S): GnRH-a treatment significantly reduced expressions of VEGF, VEGFR-1, and VEGFR-2 both in mRNA and protein levels in the ovaries of hyperstimulated rats. GnRH-a treatment also reduced vascular permeability in the ovaries of hyperstimulated rats.
CONCLUSION(S): It is speculated that GnRH-a treatment may prevent early OHSS by reducing vascular permeability through the decrease in VEGF and its receptors.
利用超刺激大鼠,阐明促性腺激素释放激素激动剂(GnRH-a)治疗预防早期卵巢过度刺激综合征(OHSS)的机制。
以超刺激大鼠作为早期OHSS模型,采用蛋白质免疫印迹分析、Northern印迹杂交和血管通透性测定的描述性研究。
实验性实验室研究。
使用Sprague-Dawley雌性大鼠收集卵巢样本。
超刺激大鼠从注射孕马血清促性腺激素(PMSG)开始至注射人绒毛膜促性腺激素(hCG)后2天连续接受GnRH-a治疗。
血管内皮生长因子(VEGF)、VEGF受体-1(VEGFR-1:Flt-1)、VEGF受体-2(VEGFR-2:KDR/Flk-1)的表达以及伊文思蓝渗漏法检测的血管通透性。
GnRH-a治疗显著降低了超刺激大鼠卵巢中VEGF、VEGFR-1和VEGFR-2在mRNA和蛋白质水平的表达。GnRH-a治疗还降低了超刺激大鼠卵巢的血管通透性。
推测GnRH-a治疗可能通过降低VEGF及其受体水平从而降低血管通透性来预防早期OHSS。