Luteinizing Hormone Releasing Hormone (LH-RH), salmon
(Synonyms: Salmon GnRH; Salmon gonadotropin-releasing hormone; sGnRH) 目录号 : GC31502
LuteinizingHormoneReleasingHormone(LH-RH),salmon是在下丘脑中合成的垂体前体十肽，在控制生殖功能中起关键作用。
Cas No.:86073-88-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Luteinizing Hormone Releasing Hormone (LH-RH), salmon is the hypophysiotropic decapeptide synthesized in the hypothalamus that plays a crucial role in the control of reproductive functions.
Luteinizing hormone-releasing hormone (LHRH) is the key hormone in the control of reproductive functions.LHRH acts as an antimitogenic factor through the activation of the Gi-cAMP intracellular signaling pathway. LHRH might act as an inhibitory factor on both cell proliferation and metastatic behavior in melanoma cells[1]. The hypothalamic decapeptide luteinizing hormone-releasing hormone (LHRH) plays a central role in the control of reproduction by stimulating the release of pituitary luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn promote gonadal functions and regulate sex steroid secretion. The effects of LHRH are mediated by high-affinity G protein-coupled LHRH-receptor (LHRH-R) on pituitary gonadotropes. The responses to LHRH vary under different conditions and critically depend on the regimens of administration and doses delivered to gonadotrope cells[2].
[1]. Moretti RM, et al. Inhibitory activity of luteinizing hormone-releasing hormone on tumor growth and progression. Endocr Relat Cancer. 2003 Jun;10(2):161-7. [2]. Horvath JE, et al. Effects of long-term treatment with the luteinizing hormone-releasing hormone (LHRH) agonist Decapeptyl and the LHRH antagonist Cetrorelix on the levels of pituitary LHRH receptors and their mRNA expression in rats. Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15048-53.
| Cas No. | 86073-88-3 | SDF | |
| 别名 | Salmon GnRH; Salmon gonadotropin-releasing hormone; sGnRH | ||
| Canonical SMILES | {Glp}-His-Trp-Ser-Tyr-Gly-Trp-Leu-Pro-Gly-NH2 | ||
| 分子式 | C60H73N15O13 | 分子量 | 1212.31 |
| 溶解度 | Soluble in Water | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.8249 mL | 4.1244 mL | 8.2487 mL |
| 5 mM | 0.165 mL | 0.8249 mL | 1.6497 mL |
| 10 mM | 0.0825 mL | 0.4124 mL | 0.8249 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
A radioimmunoassay specific for [Gln8]LH-RH: application in the confirmation of the structure of chicken hypothalamic luteinizing hormone-releasing hormone
In the first report on the chemical structure of a nonmammalian LH-RH, chicken hypothalamic LH-RH was demonstrated to be [Gln8]LH-RH [2-4]. However, these studies and subsequent reports [7,8] did not totally exclude the possibility of a reverse sequence of the two amino acids Leu-Gln. In view of the recently described structure of salmon brain LH-RH as [Trp7,Leu8]LH-RH [9], we undertook to confirm our earlier conclusion that chicken LH-RH is [Gln8]LH-RH and not [Gln7, Leu8]LH-RH. The immunologic, chromatographic and biological properties of natural chicken hypothalamic LH-RH were compared with those of the two synthetic peptides, [Gln8]LH-RH and [Gln7,Leu8]LH-RH. A radioimmunoassay highly specific for [Gln8]LH-RH was developed. Natural chicken LH-RH cross-reacted fully with the antiserum which requires the COOH-terminal Gln8 to Gly10-NH2 for binding, while [Gln7,Leu8]LH-RH showed less than 0.1% cross-reaction. On a high resolution reverse phase high performance liquid chromatography system, natural chicken LH-RH co-eluted with [Gln8]LH-RH and was well separated from [Gln7,Leu8]LH-RH. In a chicken anterior pituitary cell bioassay, natural chicken LH-RH and [Gln8]LH-RH were equipotent in stimulating luteinizing hormone release, while the relative potency of [Gln7,Leu8]LH-RH was 4.4%. These data, in particular the use of a specific [Gln8]LH-RH antiserum, provide conclusive evidence that chicken LH-RH is [Gln8]LH-RH.
Growth hormone-releasing hormone stimulates GH release while inhibiting ghrelin- and sGnRH-induced LH release from goldfish pituitary cells
Goldfish GH-releasing hormone (gGHRH) has been recently identified and shown to stimulate GH release in goldfish. In goldfish, neuroendocrine regulation of GH release is multifactorial and known stimulators include goldfish ghrelin (gGRLN19) and salmon gonadotropin-releasing hormone (sGnRH), factors that also enhance LH secretion. To further understand the complex regulation of pituitary hormone release in goldfish, we examined the interactions between gGHRH, gGRLN19, and sGnRH on GH and LH release from primary cultures of goldfish pituitary cells in perifusion. Treatment with 100nM gGHRH for 55min stimulated GH release. A 5-min pulse of either 1nM gGRLN19 or 100nM sGnRH induced GH release in na?ve cells, and these were just as effective in cells receiving gGHRH. Interestingly, gGHRH abolished both gGRLN19- and sGnRH-induced LH release and reduced basal LH secretion levels. These results suggest that gGHRH does not interfere with sGnRH or gGRLN19 actions in the goldfish somatotropes and further reveal, for the first time, that GHRH may act as an inhibitor of stimulated and basal LH release by actions at the level of pituitary cells.
Effects of a gonadotropin-releasing hormone antagonist on gonadotropin levels in Masu salmon and Sockeye salmon
The salmon gonadotropin-releasing hormone (sGnRH) is considered to be involved in gonadal maturation via gonadotropin (GTH) secretion in salmonid fishes. However, there is no direct evidence for endogenous sGnRH-stimulated GTH secretion in salmonids. In this study, to clarify whether endogenous sGnRH stimulates GTH secretion, we examined the effects of the mammalian GnRH (mGnRH) antagonist [Ac-Delta(3)-Pro(1), 4FD-Phe(2), D-Trp(3,6)]-mGnRH on luteinizing hormone (LH) levels in 0-year-old masu salmon Oncorhynchus masou and sockeye salmon Oncorhynchus nerka. First, the effects of the GnRH antagonist on LH release were examined in 0-year-old precocious male masu salmon. GnRH antagonist treatment for 3 hr significantly inhibited an increase in plasma LH levels that was artificially induced by exogenous sGnRH administration, indicating that the GnRH antagonist is effective in inhibiting LH release from the pituitary. Subsequently, we examined the effect of the GnRH antagonist on LH synthesis in 0-year-old immature sockeye salmon that were pretreated with exogenous testosterone for 42 days to increase the pituitary LH contents; the testosterone treatment did not affect the plasma LH levels. GnRH antagonist treatment slightly but significantly inhibited an increase in the testosterone-stimulated pituitary LH content levels. However, no significant differences in the plasma LH levels were observed between the GnRH antagonist-treated and control groups. These results suggest that endogenous sGnRH is involved in LH secretion in salmonid fishes.
In vitro thyrotropin-releasing activity of corticotropin-releasing hormone-family peptides in coho salmon, Oncorhynchus kisutch
Investigations of hypothalamic regulation of fish thyrotropin (TSH) secretion and subsequent thyroid activity have been impeded by the lack of a reliable assay for TSH. Using a recently developed radioimmunoassay (RIA) for coho salmon TSH we employed an in vitro pituitary cell culture technique to examine regulation of TSH secretion by corticotropin-releasing hormone (CRH) family peptides [ovine CRH (oCRH), carp urotensin I (UI), and frog sauvagine (SV)] as well as thyrotropin-releasing hormone (TRH), salmon growth hormone-releasing hormone (sGHRH), and salmon gonadotropin-releasing hormone (sGnRH). At concentrations of 0.01 to 100 nM, TRH, sGHRH, and sGnRH did not stimulate TSH secretion from coho salmon pituitary cells. However, at these same concentrations, both oCRH and SV caused a significant and concentration-dependent increase in TSH secretion; whereas, UI was highly stimulatory at all concentrations tested. In a related experiment we examined the effect of alpha-helical CRF(9-41) on oCRH-stimulated TSH release by pituitary cells. alpha-Helical CRF(9-41) is an analogue of CRH that has been shown by others to antagonize the adrenocorticotropic hormone (ACTH)-releasing activity of CRH in goldfish. Preincubation of cells with 1 microM alpha-helical CRF(9-41) for 4 h caused a significant suppression of the TSH-releasing activity of oCRH at 1.0 and 10 nM concentrations. The results of these experiments demonstrate the potency of a CRH-like peptide in the hypothalamic regulation of TSH in fish and reveal similarities in the inhibition of the response of both the thyroid and interrenal axis of fish to alpha-helical CRF(9-41).
Chicken II luteinizing hormone-releasing hormone inhibits the M-current of bullfrog sympathetic neurons
The M-current of dissociated bullfrog sympathetic neurons, measured by the whole-cell patch clamp technique, is powerfully inhibited by chicken II LH-RH (luteinizing hormone-releasing hormone), with 50% inhibition near 1 nM. Chicken II LH-RH is approximately 100 times more potent than salmon LH-RH, and at least 1000 times more potent than other known naturally occurring LH-RH analogs (chicken I LH-RH, mammalian LH-RH, and lamprey LH-RH). This high potency makes chicken II LH-RH a candidate for the endogenous transmitter mediating the late, slow excitatory postsynaptic potential (EPSP) in bullfrog sympathetic ganglia.