GnRH-I is a neuropeptide capable of regulating the release of gonadotropins, used to modulate the physiological functions of the reproductive system[1]. GnRH-I stimulates the anterior pituitary to release gonadotropins, thereby regulating the synthesis and secretion of gonadal hormones and maintaining reproductive endocrine balance[2]. GnRH-I can be used to study the regulatory mechanisms of the hypothalamic-pituitary-gonadal (HPG) axis and its role in reproductive-related diseases[3]. GnRH-I may also play a significant role in the growth of ovarian tumors[4].
In vitro, GnRH-I (3nM) stimulation of gonadotropin cells from neonatal rat pituitary for 3 hours significantly promotes the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This process depends on the activation of intracellular calcium signaling and cyclic nucleotide signaling pathways[5]. Treatment of human extravillous cytotrophoblasts (EVTs) with GnRH-I (0.1–100nM) for 24 hours significantly upregulates the mRNA and protein expression levels of urokinase-type plasminogen activator (uPA), while downregulating the expression of plasminogen activator inhibitor-1 (PAI-1). This enhances extracellular matrix degradation capacity, thereby promoting the invasive potential of trophoblast cells during early pregnancy[6].
In vivo, a single intravenous bolus of GnRH-I (0.01–10μg/kg body weight) administered to female rhesus monkeys aged 8–12 months and 21–23 months significantly promotes the release of plasma luteinizing hormone (LH), with younger individuals showing greater sensitivity[7].
References:
[1] Cheng CK, Leung PC. Molecular biology of gonadotropin-releasing hormone (GnRH)-I, GnRH-II, and their receptors in humans. Endocr Rev. 2005 Apr;26(2):283-306.
[2] Leung PC, Cheng CK, Zhu XM. Multi-factorial role of GnRH-I and GnRH-II in the human ovary. Mol Cell Endocrinol. 2003 Apr 28;202(1-2):145-53.
[3] Kern J, Schilling D, Schneeweis C, et al. Identification of the unfolded protein response pathway as target for radiosensitization in pancreatic cancer. Radiother Oncol. 2024 Feb;191:110059.
[4] Kang SK, Choi KC, Yang HS, et al. Potential role of gonadotrophin-releasing hormone (GnRH)-I and GnRH-II in the ovary and ovarian cancer. Endocr Relat Cancer. 2003 Jun;10(2):169-77.
[5] Balík A, Jindřichová M, Bhattacharyya S, et al. GnRH-I and GnRH-II-induced calcium signaling and hormone secretion in neonatal rat gonadotrophs. Physiol Res. 2009;58(5):709-716.
[6] Chou CS, Zhu H, Shalev E, et al. The effects of gonadotropin-releasing hormone (GnRH) I and GnRH II on the urokinase-type plasminogen activator/plasminogen activator inhibitor system in human extravillous cytotrophoblasts in vitro. J Clin Endocrinol Metab. 2002 Dec;87(12):5594-603.
[7] Densmore VS, Urbanski HF. Relative effect of gonadotropin-releasing hormone (GnRH)-I and GnRH-II on gonadotropin release. J Clin Endocrinol Metab. 2003 May;88(5):2126-34.
GnRH-I一种能够调节促性腺激素释放的神经肽，用于调控生殖系统的生理功能[1]。GnRH-I可以刺激垂体前叶释放促性腺激素，进而调节性腺激素的合成与分泌，维持生殖内分泌平衡[2]。GnRH-I可用于研究下丘脑-垂体-性腺轴的调控机制，以及其在生殖相关疾病中的作用[3]。GnRH-I还可能在卵巢肿瘤生长中发挥重要作用[4]。
在体外，GnRH-（3nM刺激新生大鼠垂体促性腺激素细胞3小时，显著促进促黄体生成素（LH）和促卵泡激素（FSH）的分泌，该过程依赖于激活了细胞内钙信号和环核苷酸信号通路[5]。GnRH-I（0.1–100nM）处理人绒毛外细胞滋养层细胞（EVTs）24小时，显著上调尿激酶型纤溶酶原激活物（uPA）的mRNA和蛋白表达水平，同时下调纤溶酶原激活物抑制剂-1（PAI-1）的表达，增强细胞外基质降解能力，从而促进滋养层细胞在妊娠早期的侵入潜能[6]。
在体内，GnRH-I（0.01–10μg/kg体重）单次静脉推注处理8–12月龄和21–23月龄雌性恒河猴，可显著促进血浆黄体生成素（LH）的释放，且年轻个体反应更敏感[7]。