Thyrotropin-Releasing Hormone (TRH), Free Acid (TRH-OH)
(Synonyms: 促甲状腺素释放激素游离酸,TRH-OH) 目录号 : GC31130
A tropic hormone
Cas No.:24769-58-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Thyrotropin-releasing Hormone (TRH) is a tropic hormone that stimulates release of thyroid-stimulating hormone (TSH) and prolactin.1 It binds to the human TRH receptor (TRHR) expressed in CHO cells and to rat TRHR in rat brain membranes (IC50s = 25 and 198 nM, respectively).2,3 TRH (1 μM) decreases polyphosphoinositide and increases arachidonic and oleic acid diacylglycerol incorporation into lipids of GH3 rat pituitary tumor cells.4 In vitro, it dose-dependently increases TSH release from rat anterior pituitary slices and prolactin release from cultured anterior pituitary cells.5,6 In vivo, TRH (0.01 mg/kg) increases TSH and prolactin plasma levels in rats.1
1.Dettmar, P.W., Lynn, A.G., Metcalf, G., et al.The ability of RX 77368 - a stabilised analogue of TRH - to provoke the secretion of prolactin and TSH in vivoNeuropeptides3(1)1-8(1982) 2.Yamada, M., Iwasaki, T., Satoh, T., et al.Activation of the thyrotropin-releasing hormone (TRH) receptor by a direct precursor of TRH, TRH-GlyNeurosci. Lett.196(1-2)109-112(1995) 3.Bhargava, H.N., and Das, S.Evidence for opiate action at the brain receptors for thyrotropin-releasing hormoneBrain Res.368(2)262-267(1986) 4.Martin, T.F.J.Thyrotropin-releasing hormone rapidly activates the phosphodiester hydrolysis of polyphosphoinositides in GH3 pituitary cells. Evidence for the role of a polyphosphoinositide-specific phospholipase C in hormone actionJ. Biol. Chem.258(24)14816-14822(1983) 5.Iriuchijima, T., Michimata, T., Miyashita, K., et al.Thyroid hormones regulate the formation of inositol phosphate in response to thyrotropin-releasing hormone in rat anterior pituitariesNeuropeptides21(1)49-53(1992) 6.Apfelbaum, M.E.Role of vasoactive intestinal peptide and 5-HT2 receptor subtype in serotonin stimulation of basal and thyrotropin-releasing-hormone-induced prolactin release in vitro from rat pituitary cellsNeuroendocrinology67(1)45-50(1998)
| Cas No. | 24769-58-2 | SDF | |
| 别名 | 促甲状腺素释放激素游离酸,TRH-OH | ||
| Canonical SMILES | {pGlu}-His-Pro | ||
| 分子式 | C16H21N5O5 | 分子量 | 363.37 |
| 溶解度 | H2O : 100 mg/mL (275.20 mM; Need ultrasonic) | 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 | 2.752 mL | 13.7601 mL | 27.5202 mL |
| 5 mM | 0.5504 mL | 2.752 mL | 5.504 mL |
| 10 mM | 0.2752 mL | 1.376 mL | 2.752 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。
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Thyroliberin (TRH) and TRH free acid (TRH-OH) present in milk do not originate from local synthesis in mammary gland
Hypothalamic hormones represent a peculiar group of hormones present in milk in surprisingly high concentrations. High levels of these neuropeptides raised the question of their origin. The hypothesis suggesting local synthesis of TRH in the mammary gland was, therefore, tested. Acid extracts of human milk contained TRH and TRH-OH immunoreactivity. RIA determinations at various purification steps revealed that only a part of the immunoreactivity may represent authentic peptides. No high molecular weight TRH precursor could be demonstrated upon a sequential enzymatic treatment of human milk and rat mammary gland extracts. Exploration of rat mammary gland tissue for TRH mRNA showed that the TRH gene is not expressed in the mammary gland. Rat mammary gland homogenates were able to deamidate exogenous TRH to TRH-OH. Conclusion: TRH is not synthesized in the mammary gland via a high molecular weight precursor. It is likely that the TRH-free acid in milk (demonstrated for the first time in this product) originates from TRH deamidation in mammary gland cells during TRH transport from the blood.
Degradation of thyrotropin releasing hormone and a related compound by rat liver and kidney homogenate
The inactivation of the hypothalamic hormone by rat liver and kidney homogenates was studied, using specific radioimmunoassays for the measurement of thyrotropin releasing hormone, pGlu-His-Pro-NH2 (TRH), and for an analogous peptide, pGlu-His-Pro-OH(TRH-OH), which has been proposed as a major metabolite of TRH [NAIR et al., 1971]. The inactivation of TRH and the free acid was found to be rapid. Heat lability and saturation kinetics suggest the involvement of enzymatic processes. In liver homogenate, TRH-OH production from TRH was observed. The accumulation of TRH-OH was substantial in experiments employing near-saturation concentrations of TRH. The liver and kidney are ascribed as major sites for breakdown of TRH in vivo.
The involvement of central cholinergic mechanisms in cardiovascular responses to intracerebroventricular and intravenous administration of thyrotropin-releasing hormone
Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) in a range from 0.1 to 100 micrograms induced a dose-related increase in blood pressure in conscious rats, whereas TRH-free acid (TRH-OH) and histidyl-proline diketopiperazine (His-Pro-DKP), metabolites of TRH, did not. The blood pressure responses to intravenous (i.v.) injection of 5 mg/Kg TRH were similar to those induced by TRH (i.c.v.). Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH administered through either route. Hemicholinium-3 (50 micrograms, i.c.v.), an inhibitor of choline uptake, also prevented the increase in blood pressure induced by TRH (10 micrograms, i.c.v.). These results indicate that both centrally and peripherally administered TRH have pressor effects that are mediated by central cholinergic mechanisms, probably by activating cholinergic neurons.